A 25-year-old man has an isolated decrease in glomerular filtration rate (GFR) following constriction of the afferent arteriole. Which of the following changes is most likely to occur immediately after the constriction?
A. Decreased glomerular capillary hydrostatic pressure
B. Increased filtration fraction
C. Increased renal plasma flow (RPF)
D. Increased peritubular capillary hydrostatic pressure
E. Increased oncotic pressure in Bowman's space
Answer: A
Explanation: Afferent arteriole constriction decreases hydrostatic pressure in glomerular capillaries → lower GFR. RPF falls, FF (GFR/RPF) may decrease or remain same depending; peritubular hydrostatic pressure is not increased. Oncotic pressure in Bowman's space is normally ~0.
Which transporter in the proximal tubule is primarily responsible for the majority of filtered bicarbonate reclamation?
A. Na⁺/H⁺ exchanger (NHE3) on apical membrane
B. H⁺-ATPase on apical membrane
C. Pendrin (Cl⁻/HCO₃⁻ exchanger) on basolateral membrane
D. Na⁺/K⁺ ATPase on apical membrane
E. ROMK channel on apical membrane
Answer: A
Explanation: Reabsorption of filtered HCO₃⁻ in proximal tubule: apical NHE3 secretes H⁺ into lumen where it combines with filtered HCO₃⁻ forming CO₂, which crosses cells and is converted back to HCO₃⁻ transported to blood. Na⁺/K⁺ ATPase is basolateral. Pendrin is type B intercalated cells in collecting duct.
A patient with congestive heart failure develops prerenal azotemia. Which of the following lab patterns is most consistent with prerenal azotemia?
A. Fractional excretion of sodium (FeNa) > 2%
B. Urine sodium < 20 mEq/L, BUN:Cr ratio > 20:1
C. Urine osmolality ≈ plasma osmolality (~300 mOsm/kg)
D. Intrinsic renal damage on urine sediment with muddy brown casts
E. Metabolic alkalosis due to ammoniagenesis
Answer: B
Explanation: Prerenal azotemia: low renal perfusion leads to avid Na⁺ and water retention → urine Na⁺ low (<20), FeNa <1%, urine osm high (>500), BUN:Cr >20 due to increased urea reabsorption.
Which diuretic acts on the thick ascending limb of the loop of Henle by inhibiting the Na⁺-K⁺-2Cl⁻ cotransporter (NKCC2)?
A. Furosemide
B. Hydrochlorothiazide
C. Spironolactone
D. Acetazolamide
E. Amiloride
Answer: A
Explanation: Loop diuretics (furosemide, bumetanide, torsemide) inhibit NKCC2 in TAL → impair countercurrent multiplication, decrease medullary hypertonicity, cause Ca²⁺/Mg²⁺ loss.
(Clinical vignette) A 48-year-old diabetic man with long-standing poorly controlled diabetes presents with proteinuria (6 g/day), hypercholesterolemia, hypoalbuminemia, and edema. Which is the most likely diagnosis?
A. Minimal change disease
B. Focal segmental glomerulosclerosis (FSGS)
C. Membranous nephropathy
D. Diabetic nephropathy (nodular glomerulosclerosis)
E. Acute poststreptococcal glomerulonephritis
Answer: D
Explanation: Long-standing diabetes → diabetic nephropathy with nodular (Kimmelstiel-Wilson) glomerulosclerosis and progressive proteinuria, often nephrotic range. Membranous causes nephrotic syndrome in adults but diabetes fits better.
Which acid–base disorder is expected in a patient with vomiting?
A. Metabolic acidosis with high anion gap
B. Metabolic acidosis with normal anion gap
C. Metabolic alkalosis with increased bicarbonate and volume contraction
D. Respiratory acidosis due to hypoventilation
E. Respiratory alkalosis due to hyperventilation
Answer: C
Explanation: Vomiting leads to loss of HCl → metabolic alkalosis. Volume contraction increases bicarbonate reabsorption (contraction alkalosis). Kidneys may conserve Cl⁻ leading to hypochloremic metabolic alkalosis.
A renovascular hypertension patient has unilateral renal artery stenosis. Which hormone change would you expect from the affected kidney?
A. Decreased renin secretion
B. Increased renin secretion
C. Increased atrial natriuretic peptide release
D. Increased ADH release from posterior pituitary
E. Decreased aldosterone secretion
Answer: B
Explanation: Reduced renal perfusion pressure sensed by JG cells → increased renin → activation of RAAS → systemic hypertension.
Which of the following best describes renal handling of a substance that is freely filtered, not reabsorbed, and secreted at the proximal tubule?
A. Clearance equals inulin clearance
B. Clearance less than inulin clearance but greater than zero
C. Clearance greater than inulin clearance
D. Clearance greater than renal plasma flow
E. Clearance equal to zero
Answer: C
Explanation: If substance is filtered + secreted, clearance > inulin clearance (GFR). It cannot exceed RPF maximum depending on secretion but in theory secreted substances (PAH) have clearance approximating RPF.
Which of the following antibodies is most commonly associated with membranous nephropathy in adults?
A. Anti-phospholipase A2 receptor (anti-PLA2R)
B. Anti-GBM antibodies
C. ANCA
D. Anti-dsDNA antibodies
E. Anti-PLA1 receptor
Answer: A
Explanation: Primary membranous nephropathy is associated with anti-PLA2R antibodies (podocyte antigen). Anti-GBM → Goodpasture; ANCA → pauci-immune GN.
An 18-year-old has a mutation in aquaporin-2 channel causing nephrogenic diabetes insipidus. Which of the following is true?
A. Water reabsorption in collecting duct increases when ADH present
B. Patient will concentrate urine after desmopressin (ADH analog)
C. Serum sodium tends to fall (hyponatremia)
D. Urine osmolality is low and does not respond to ADH
E. Kidney responds normally to ADH
Answer: D
Explanation: Nephrogenic DI: collecting duct insensitive to ADH → inability to concentrate urine; desmopressin does not increase urine osmolality. Serum sodium may increase if free water lost.
In the countercurrent multiplication system, which segment is impermeable to water but reabsorbs NaCl actively?
A. Proximal tubule
B. Descending limb of loop of Henle
C. Thin ascending limb
D. Thick ascending limb
E. Collecting duct
Answer: D
Explanation: Thick ascending limb (TAL) is impermeable to water and actively reabsorbs NaCl via NKCC2; this creates the cortico-medullary gradient.
Which urinary finding is most characteristic of acute tubular necrosis (ATN)?
A. RBC casts
B. White cell casts
C. Fatty casts (oval fat bodies)
D. Muddy brown granular casts
E. Waxy casts
Answer: D
Explanation: ATN causes sloughed tubular epithelial cells forming muddy brown granular casts. RBC casts → glomerulonephritis; fat bodies → nephrotic syndrome; waxy casts → chronic renal failure.
(Clinical vignette) A 35-year-old woman presents with flank pain; urinalysis shows calcium oxalate crystals. Which of the following will most reduce formation of these stones?
A. Increase dietary oxalate
B. Thiazide diuretics
C. Carbonic anhydrase inhibitors
D. Loop diuretics
E. High-protein diet
Answer: B
Explanation: Thiazides reduce urinary calcium excretion by increasing proximal tubular Ca²⁺ reabsorption → lower urinary Ca²⁺ and reduce recurrent calcium kidney stones. Carbonic anhydrase inhibitors increase risk by alkalinizing urine.
Which acid–base change occurs with loop diuretics like furosemide?
A. Metabolic acidosis due to HCO₃⁻ loss
B. Metabolic alkalosis due to contraction and increased aldosterone
C. Respiratory acidosis
D. Hyperchloremic metabolic acidosis
E. Mixed respiratory and metabolic alkalosis
Answer: B
Explanation: Loop diuretics cause volume contraction, increased aldosterone, enhanced H⁺ and K⁺ secretion → metabolic alkalosis (contraction alkalosis).
Which segment is the predominant site for glucose reabsorption under normal conditions?
A. Proximal convoluted tubule via SGLT2 and GLUT2
B. Proximal convoluted tubule via SGLT1 and GLUT1 only
C. Thick ascending limb via SGLT2
D. Distal tubule via SGLT1
E. Collecting duct via facilitated diffusion
Answer: A
Explanation: Majority of filtered glucose reabsorbed in early PCT via SGLT2 (low affinity, high capacity) and basolateral GLUT2. SGLT1 in late PCT contributes minor amount.
A patient with chronic metabolic acidosis will increase which renal process to compensate?
A. Decrease ammoniagenesis in proximal tubule
B. Increase HCO₃⁻ excretion
C. Increase renal NH₄⁺ excretion (ammoniagenesis) and HCO₃⁻ generation
D. Decrease H⁺ secretion in collecting duct
E. Reduce distal HCO₃⁻ regeneration
Answer: C
Explanation: Chronic metabolic acidosis → kidney increases ammoniagenesis (glutamine metabolism) to excrete NH₄⁺ and regenerate HCO₃⁻, aiding acid excretion.
A patient has a defect in the H⁺/K⁺ ATPase in alpha-intercalated cells. Which electrolyte abnormality is likely?
A. Hyperkalemia with metabolic acidosis
B. Hypokalemia with metabolic alkalosis
C. Hypokalemia with metabolic acidosis
D. Hyperkalemia with metabolic alkalosis
E. No change in K⁺ handling
Answer: C
Explanation: H⁺/K⁺ ATPase secretes H⁺ in exchange for K⁺ uptake; defect reduces H⁺ secretion → metabolic acidosis. Also reduces K⁺ reabsorption, sometimes causing hypokalemia? Actually loss of H⁺ secretion often causes hyperkalemia, but with defective H⁺/K⁺ pump specifically, less K⁺ reabsorbed → hypokalemia. This is a more complex niche Q; the net effect typically is metabolic acidosis and hyperkalemia when distal H⁺ secretion is impaired. But the H⁺/K⁺ ATPase contributes to K⁺ uptake; its loss tends to reduce K⁺ reabsorption → hypokalemia. For exam clarity: defect gives metabolic acidosis and hypokalemia.
(Note: this item is intentionally challenging — the usual clinical pattern with impaired distal H⁺ secretion (e.g., type 1 RTA) is metabolic acidosis with hypokalemia due to secondary effects and increased K⁺ excretion.)
A 50-year-old man is given an ACE inhibitor. Which of the following lab changes is most expected?
A. Decrease in serum potassium
B. Increase in efferent arteriole constriction
C. Decrease in aldosterone secretion
D. Increased angiotensin II formation
E. Increased GFR due to efferent arteriole constriction
Answer: C
Explanation: ACE inhibitors reduce angiotensin II → decreased aldosterone → risk of hyperkalemia. They dilate efferent arteriole (decrease constriction) → can lower GFR.
Which molecule is most likely elevated in minimal change disease?
A. Circulating anti-PLA2R antibodies
B. Cytokine(s) causing podocyte foot process effacement (e.g., IL-13)
C. Immune complex deposition along GBM
D. Linear IgG deposition
E. ANCA antibodies
Answer: B
Explanation: Minimal change disease is thought to be T-cell mediated with cytokines (e.g., IL-13) causing podocyte effacement and selective albuminuria. No immune complex deposition.
Which acid–base disorder is seen in primary hyperaldosteronism?
A. Hyperkalemic metabolic acidosis
B. Hypokalemic metabolic alkalosis
C. Hypokalemic metabolic acidosis
D. Hypernatremic metabolic acidosis
E. Respiratory alkalosis
Answer: B
Explanation: Excess aldosterone → increased Na⁺ reabsorption and K⁺ and H⁺ secretion → hypokalemia and metabolic alkalosis.
Which urinary buffer increases in the lumen when the kidney excretes a net acid load chronically?
A. Bicarbonate
B. Phosphate (titratable acid) and ammonium (NH₄⁺)
C. Urea
D. Creatinine
E. Albumin
Answer: B
Explanation: Chronic acid excretion increases titratable acids (HPO₄²⁻ → H₂PO₄⁻) and ammonium excretion (NH₄⁺), both key urinary buffers.
(Clinical vignette) A 30-year-old woman with systemic lupus erythematosus presents with nephritic urine sediment, hematuria, and RBC casts. Anti-dsDNA titers are high. Which glomerular lesion is most likely?
A. Membranous nephropathy
B. Diffuse proliferative glomerulonephritis (diffuse proliferative GN)
C. Focal segmental glomerulosclerosis
D. Minimal change disease
E. IgA nephropathy
Answer: B
Explanation: SLE classically produces diffuse proliferative GN (WHO class IV) with “wire-loop” immune complex deposits and nephritic presentation; anti-dsDNA often correlates.
The glomerular filtration barrier includes all EXCEPT:
A. Fenestrated endothelium
B. Glomerular basement membrane (GBM) with heparan sulfate
C. Podocyte foot processes and slit diaphragm
D. Mesangial cell slit diaphragm
E. Negatively charged glycoprotein coating
Answer: D
Explanation: Mesangial cells provide support and phagocytosis but are not part of the filtration slit. Filtration barrier = fenestrated endothelium + GBM + podocyte foot processes/slit diaphragm.
Which change in the nephron increases calcium reabsorption?
A. Loop diuretics
B. Thiazide diuretics
C. Carbonic anhydrase inhibitors
D. Increased ECF volume
E. Inhibition of NCC in DCT
Answer: B
Explanation: Thiazides increase Ca²⁺ reabsorption in DCT (by increasing transcellular Ca²⁺ reabsorption secondary to decreased intracellular Na⁺). Loop diuretics increase Ca²⁺ excretion.
A patient has metabolic acidosis with an anion gap of 28 mEq/L and osmolar gap elevation. Which toxin is most probable?
A. Methanol or ethylene glycol ingestion
B. Aspirin overdose only causes respiratory alkalosis
C. Uremia (renal failure) but no osm gap
D. Diarrhea causes high anion gap
E. Primary hyperaldosteronism
Answer: A
Explanation: High anion gap metabolic acidosis with osmolar gap suggests ingestion of methanol or ethylene glycol (toxic alcohols). Uremia causes HAGMA but not osmolar gap.
Which of the following is the major stimulus for ADH (vasopressin) release?
A. Decreased plasma osmolality
B. Increased plasma osmolality detected by hypothalamic osmoreceptors
C. Increased blood pressure
D. Decreased RAAS activation
E. Increased atrial stretch
Answer: B
Explanation: Increased plasma osmolality is the primary stimulus for ADH secretion; hypotension/hypovolemia also stimulate ADH via baroreceptors.
Which renal pathology classically causes hypercellular glomeruli with granular IgG and complement deposition on IF and “lumpy-bumpy” appearance?
A. Acute poststreptococcal glomerulonephritis
B. Membranous nephropathy
C. Minimal change disease
D. Focal segmental glomerulosclerosis
E. Diabetic nephropathy
Answer: A
Explanation: Post-streptococcal GN shows hypercellular glomeruli and granular (“lumpy-bumpy”) deposits of IgG, IgM, C3 along GBM.
Which transporter is inhibited by SGLT2 inhibitors (e.g., empagliflozin) and what is a downstream renal effect?
A. Inhibits SGLT2 → decreases glycosuria
B. Inhibits SGLT2 → decreases proximal Na⁺ reabsorption and may increase distal tubule Na⁺ delivery → modest natriuresis
C. Inhibits NKCC2 → increase calcium reabsorption
D. Inhibits ENaC → hyperkalemia
E. Inhibits pendrin → metabolic acidosis
Answer: B
Explanation: SGLT2 inhibitors block proximal glucose/Na⁺ cotransport → glucosuria and less Na⁺ reabsorption proximally → increased distal Na⁺ delivery, modest natriuresis and diuretic-like effects.
Which of the following best characterizes Fanconi syndrome?
A. Proximal tubular dysfunction causing glycosuria, aminoaciduria, phosphaturia, bicarbonaturia
B. Distal RTA type I with impaired acid secretion
C. Isolated aldosterone deficiency
D. Thick ascending limb dysfunction only
E. Collecting duct AVP receptor abnormality
Answer: A
Explanation: Fanconi syndrome = generalized proximal tubule reabsorption defect → loss of glucose, amino acids, phosphate, bicarbonate, leading to proximal RTA (type 2) and hypophosphatemic rickets/osteomalacia.
Which of the following reduces renal ammoniagenesis and can impair acid excretion?
A. Hypokalemia
B. Chronic metabolic acidosis
C. Mineralocorticoid excess (aldosterone)
D. Hypoaldosteronism (low aldosterone)
E. Increased glutamine delivery to proximal tubule
Answer: D
Explanation: Hypoaldosteronism reduces distal H⁺ and NH₄⁺ excretion and reduces ammoniagenesis indirectly; hypokalemia increases ammoniagenesis. Chronic acidosis stimulates it.
(Clinical vignette) A 40-year-old alcoholic presents with severe flank pain and radiolucent kidney stones on x-ray. Urinalysis shows needle-shaped crystals. Which stone is most likely?
A. Calcium oxalate
B. Struvite (Mg-ammonium-phosphate)
C. Uric acid stone
D. Cystine stone
E. Calcium phosphate
Answer: C
Explanation: Uric acid stones are radiolucent (not seen on plain x-ray), common in acidic urine and hyperuricemia; crystals are rhomboid/needle-shaped. Calcium stones are radiopaque.
A 60-year-old man with long-term NSAID use develops minimal change-like nephrotic syndrome. Which mechanism is most plausible?
A. NSAIDs induce immune complex deposition on GBM
B. NSAIDs inhibit prostaglandin synthesis leading to reduced renal blood flow only
C. NSAIDs cause mitochondrial toxicity in podocytes
D. NSAIDs can cause minimal change disease by T-cell mediated podocyte injury and also cause membranous nephropathy; additionally NSAIDs can cause interstitial nephritis
E. NSAIDs have no renal effects
Answer: D
Explanation: NSAIDs are linked to several renal syndromes: minimal change disease (podocyte injury via immune mechanisms), membranous nephropathy, acute interstitial nephritis, and decreased prostaglandin-dependent RBF.
The filtration fraction (FF) is defined as GFR/RPF. If GFR is 120 mL/min and RPF is 600 mL/min, what is the FF?
A. 0.03
B. 0.2
C. 0.5
D. 5
E. 720
Answer: B
Explanation: FF = 120/600 = 0.2 (20%). Compute digit by digit: 120/600 = 0.2.
Which of the following immunologic findings are associated with rapidly progressive glomerulonephritis (RPGN) with linear IgG deposition?
A. Anti-GBM antibodies (Goodpasture syndrome)
B. Immune complex deposition in subepithelial humps
C. ANCA positive only
D. IgA mesangial deposition
E. Membranous thickening of GBM
Answer: A
Explanation: RPGN can be due to anti-GBM (linear IgG), immune complex (granular), or pauci-immune (ANCA) types. Goodpasture has anti-GBM linear deposits.
Which diuretic is potassium-sparing by antagonizing aldosterone receptor on principal cells?
A. Spironolactone
B. Furosemide
C. Hydrochlorothiazide
D. Mannitol
E. Acetazolamide
Answer: A
Explanation: Spironolactone (and eplerenone) are antagonists of aldosterone receptor in principal cells of collecting duct → reduce ENaC expression/activity, decrease K⁺ secretion → K⁺-sparing.
A 5-year-old with recurrent infections has nephrotic syndrome, black urine, and sensorineural deafness. Which diagnosis fits?
A. Alport syndrome (collagen IV mutation)
B. Minimal change disease
C. Goodpasture syndrome
D. IgA nephropathy
E. Membranous nephropathy
Answer: A
Explanation: Alport syndrome: mutation in type IV collagen → hematuria, progressive renal failure, sensorineural deafness, ocular abnormalities.
Which transport process in the proximal tubule is secondary active transport?
A. Glucose reabsorption via SGLT using Na⁺ gradient established by Na⁺/K⁺ ATPase
B. Bicarbonate reabsorption via basolateral HCO₃⁻ transporter directly powered by ATP
C. K⁺ secretion via ROMK using ATP
D. Filtration of plasma proteins across GBM
E. Passive diffusion of urea only
Answer: A
Explanation: SGLT uses Na⁺ gradient (maintained by basolateral Na⁺/K⁺ ATPase) to drive glucose uptake — secondary active transport.
(Clinical vignette) A patient with metastatic prostate cancer is receiving amphotericin B for systemic fungal infection and develops hypokalemia and metabolic acidosis. What renal tubular dysfunction is most consistent?
A. Type 1 (distal) RTA causing inability to acidify urine
B. Type 2 (proximal) RTA causing bicarbonate wasting and proximal tubule injury
C. Type 4 RTA causing hyperkalemia
D. Fanconi syndrome only with glycosuria
E. Postrenal obstruction
Answer: B
Explanation: Amphotericin B causes renal tubular toxicity including proximal tubular dysfunction (Fanconi syndrome) and distal dysfunction; proximal RTA (type 2) causes bicarbonate wasting, metabolic acidosis, often with hypokalemia.
Which of the following is true about PAH (para-aminohippurate) clearance?
A. PAH clearance approximates GFR
B. PAH clearance approximates renal plasma flow (RPF) at low plasma PAH concentrations
C. PAH is reabsorbed in the proximal tubule
D. PAH is filtered only, not secreted
E. PAH clearance equals inulin clearance
Answer: B
Explanation: PAH is filtered and secreted so its clearance approximates RPF when extraction is near complete (low plasma PAH). Inulin clears GFR.
Which mechanism explains why hyperglycemia in uncontrolled diabetes increases GFR (early hyperfiltration)?
A. Increased afferent arteriole constriction via sympathetic tone
B. Increased glucose in filtrate increases proximal Na⁺ reabsorption via SGLT2 → decreased Na⁺ delivery to macula densa → decreases TGF signal → afferent arteriole dilatation → increased GFR
C. Increased RAAS constricts efferent arteriole only
D. Decreased glomerular capillary hydrostatic pressure
E. Increased albuminuria reduces oncotic pressure
Answer: B
Explanation: High filtered glucose → increased proximal reabsorption (via SGLT2) reduces NaCl delivery to macula densa → tubuloglomerular feedback induces afferent dilation → hyperfiltration.
Which condition causes hypokalemia with metabolic alkalosis and hypertension due to increased mineralocorticoid effect but low aldosterone?
A. Liddle syndrome (gain of ENaC function)
B. Primary hyperaldosteronism (Conn)
C. Addison disease
D. Gitelman syndrome
E. Bartter syndrome
Answer: A
Explanation: Liddle syndrome (constitutive ENaC activity) causes increased Na⁺ reabsorption, K⁺ and H⁺ loss → hypertension, hypokalemic metabolic alkalosis, low aldosterone due to negative feedback.
A reduction in the glomerular capillary surface area (e.g., due to glomerulosclerosis) will cause which change in GFR and filtration coefficient (Kf)?
A. Decrease in GFR due to decreased Kf
B. Increase in GFR due to increased Kf
C. No change in GFR
D. Increase in RPF only
E. Decrease in oncotic pressure
Answer: A
Explanation: GFR = Kf × net filtration pressure. Loss of surface area reduces Kf → decreases GFR.
Which of the following antibiotics is most associated with interstitial nephritis?
A. Penicillins (e.g., methicillin) and sulfonamides
B. Vancomycin causing only ATN
C. Aminoglycosides causing glomerulonephritis
D. Cephalosporins are harmless to kidneys
E. Tetracyclines cause only hepato-toxicity
Answer: A
Explanation: Many antibiotics (β-lactams like methicillin, penicillins, cephalosporins, sulfonamides) can cause acute interstitial nephritis (AIN) — immune mediated interstitial inflammation.
Which of the following best describes the mechanism of action of acetazolamide?
A. Inhibits carbonic anhydrase in proximal tubule → decreased HCO₃⁻ reabsorption → bicarbonaturia and metabolic acidosis
B. Inhibits NKCC2 in TAL
C. Blocks ENaC in collecting duct
D. Antagonizes mineralocorticoid receptor
E. Blocks SGLT2
Answer: A
Explanation: Acetazolamide inhibits carbonic anhydrase in PCT → decreased HCO₃⁻ reabsorption → proximal RTA like effect and metabolic acidosis, causes diuresis and alkaline urine.
(Clinical vignette)A 28-year-old man presents with recurrent nephrolithiasis. Urine analysis shows hexagonal crystals and a positive cyanide-nitroprusside test. What is the diagnosis and inheritance?
A. Cystinuria — AR defect in dibasic amino acid transport
B. Uric acid stones — associated with gout
C. Calcium oxalate stones — due to hypocitraturia
D. Struvite stones — infection with urease-producing organisms
E. Xanthinuria — xanthine oxidase deficiency
Answer: A
Explanation: Cystinuria (autosomal recessive) → defective renal reabsorption of cystine and other dibasic AAs → cystine stones; hexagonal crystals and positive cyanide-nitroprusside test.
During severe volume depletion, which of the following changes occurs in the peritubular capillaries to favor reabsorption of fluid from interstitium into capillaries?
A. Increased peritubular capillary hydrostatic pressure
B. Decreased peritubular capillary oncotic pressure
C. Increased peritubular capillary oncotic pressure due to hemoconcentration
D. Increased interstitial hydrostatic pressure contributing to filtration
E. Increased filtered load of sodium
Answer: C
Explanation: Volume depletion concentrates plasma proteins → increases peritubular capillary oncotic pressure favoring reabsorption from interstitium into capillaries.
Which of the following is a hallmark of nephrotic syndrome?
A. Hematuria and RBC casts
B. Proteinuria >3.5 g/day, hypoalbuminemia, hyperlipidemia, edema
C. Oliguria with elevated creatinine only
D. Hypocalcemia due to Ca²⁺ loss in urine
E. Polyuria and polydipsia only
Answer: B
Explanation: Nephrotic syndrome: heavy proteinuria (>3.5 g/day), hypoalbuminemia, hyperlipidemia, edema. Hematuria is more typical of nephritic syndromes.
A drug that blocks the epithelial sodium channel (ENaC) in the principal cells will cause which of the following?
A. Increased sodium reabsorption and hypokalemia
B. Decreased sodium reabsorption and hyperkalemia
C. Increased H⁺ secretion causing metabolic alkalosis
D. Increased aldosterone secretion directly
E. Increased ammoniagenesis
Answer: B
Explanation: ENaC blockers (amiloride, triamterene) reduce Na⁺ reabsorption in collecting duct → decrease electrochemical gradient for K⁺ secretion → hyperkalemia. Reduced H⁺ secretion can lead to metabolic acidosis.
Which of the following statements about renal blood flow autoregulation is true?
A. Autoregulation maintains RBF constant only when MAP between 40–60 mmHg
B. Myogenic mechanism and tubuloglomerular feedback contribute to autoregulation of RBF between approximately 80–180 mmHg
C. Autoregulation is mediated solely by sympathetic nervous system
D. Autoregulation is absent in most healthy humans
E. RAAS is primary mechanism for minute-to-minute autoregulation
Answer: B
Explanation: Renal autoregulation via myogenic response and tubuloglomerular feedback works over MAP ~80–180 mmHg to keep RBF and GFR relatively constant. Sympathetic/RAAS act outside that.
Which electrolyte abnormality is classic for type 4 renal tubular acidosis (hyporeninemic hypoaldosteronism)?
A. Hypokalemia with metabolic alkalosis
B. Hyperkalemia with mild metabolic acidosis
C. Hypocalcemia with hyperphosphatemia
D. Severe metabolic alkalosis and hypertension
E. Hypomagnesemia only
Answer: B
Explanation: Type 4 RTA: hypoaldosteronism or resistance → decreased distal Na⁺ reabsorption and reduced K⁺ and H⁺ secretion → hyperkalemia and mild metabolic acidosis.
(Clinical vignette) A 60-year-old with long-standing hypertension now has microalbuminuria progressing to overt proteinuria. Biopsy shows hyaline arteriolosclerosis and nephrosclerosis. Which is true?
A. This is typical for benign nephrosclerosis due to chronic hypertension leading to ischemic atrophy of renal parenchyma and slowly progressing CKD
B. This is typical for diabetic nodular glomerulosclerosis only
C. Hyaline arteriolosclerosis causes increased GFR
D. It indicates acute nephritic syndrome
E. It is immunologically mediated GN
Answer: A
Explanation: Chronic benign hypertension leads to hyaline arteriolosclerosis and nephrosclerosis → chronic ischemic injury and progressive CKD with proteinuria. Not immune complex mediated.
Which of the following parameters is increased by constriction of the efferent arteriole?
A. Glomerular capillary hydrostatic pressure and GFR (initially)
B. Renal plasma flow (RPF)
C. Peritubular capillary pressure
D. Filtration fraction decreases
E. Decrease in glomerular capillary oncotic pressure
Answer: A
Explanation: Efferent arteriole constriction increases glomerular capillary hydrostatic pressure raising GFR; RPF decreases so FF (GFR/RPF) increases. Peritubular capillary pressure decreases; oncotic pressure in glomerular capillaries increases.
Which of the following metabolic changes increases tubular phosphate reabsorption in proximal tubule?
A. PTH increase
B. Low dietary phosphate and increased NaPi cotransporter expression
C. High dietary phosphate
D. FGF23 upregulation
E. Chronic kidney disease increases phosphate excretion only
Answer: B
Explanation: Low dietary phosphate upregulates NaPi cotransporters increasing proximal phosphate reabsorption. PTH and FGF23 decrease phosphate reabsorption.
Which of the following is a major effect of atrial natriuretic peptide (ANP) on the kidney?
A. Increase sodium reabsorption in collecting duct
B. Dilate afferent arteriole and constrict efferent arteriole → increase GFR and natriuresis
C. Stimulate RAAS activation
D. Increase aldosterone secretion
E. Increase ADH release
Answer: B
Explanation: ANP dilates afferent and constricts efferent arterioles → increases GFR; it inhibits Na⁺ reabsorption in collecting duct and inhibits renin/aldosterone → natriuresis.
Which of the following best explains why the late distal tubule and collecting duct are major sites for K⁺ regulation?
A. They have low permeability to K⁺
B. Principal cells have aldosterone-sensitive Na⁺ channels (ENaC) and ROMK allowing K⁺ secretion in exchange for Na⁺ reabsorption
C. PCT handles most K⁺ secretion under hormone control
D. TAL is main site of K⁺ secretion regulated by aldosterone
E. Glomerulus filters all K⁺ and no reabsorption occurs
Answer: B
Explanation: Principal cells express ENaC and ROMK; aldosterone increases Na⁺ uptake creating lumen negativity that drives K⁺ secretion via ROMK — central to K⁺ homeostasis.
(Clinical vignette) A 45-year-old woman with SLE has heavy proteinuria, and a biopsy shows immune complex deposition along the subepithelial side of GBM with thickened capillary walls and "spike and dome" appearance on electron microscopy. Which disease?
A. Membranous nephropathy
B. Minimal change disease
C. FSGS
D. IgA nephropathy
E. Diabetic nephropathy
Answer: A
Explanation: Membranous nephropathy shows subepithelial immune complexes with GBM thickening and spike-and-dome appearance. It causes nephrotic syndrome.
Which of the following best describes renal clearance?
A. Clearance = (Urine concentration × urine flow) / Plasma concentration
B. Clearance = (Plasma concentration × urine flow) / Urine concentration
C. Clearance = GFR × RPF
D. Clearance = Filtration fraction × GFR
E. Clearance cannot be measured clinically
Answer: A
Explanation: Clearance of X = (Ux × V) / Px where Ux = urine conc, V = urine flow (mL/min), Px = plasma conc.
A 70-year-old on spironolactone develops gynecomastia. Which drug is a better alternative to avoid endocrine side effects?
A. Eplerenone
B. Amiloride
C. Hydrochlorothiazide
D. Furosemide
E. Mannitol
Answer: A
Explanation: Eplerenone is a selective aldosterone receptor antagonist with less affinity for androgen/progesterone receptors than spironolactone → less gynecomastia. Amiloride is K⁺‐sparing but acts on ENaC.
Which substance is freely filtered, not reabsorbed but secreted, and is used to estimate RPF?
A. Inulin
B. Creatinine
C. PAH
D. Glucose
E. Urea
Answer: C
Explanation: PAH is filtered and secreted with near-complete extraction at low plasma levels → clearance approximates RPF. Inulin measures GFR.
Which of the following renal lesions is most associated with hepatitis B and C infections?
A. Membranous nephropathy (HBV) and MPGN (HCV)
B. Minimal change disease with HCV
C. Goodpasture syndrome with HBV
D. Alport syndrome with HCV
E. Liddle syndrome with HBV
Answer: A
Explanation: HBV associated with membranous nephropathy; HCV associated with mixed cryoglobulinemia → membranoproliferative GN (MPGN).
(Clinical vignette) A 22-year-old woman has episodic hematuria one day after URTI. She has IgA deposits in mesangium on IF. What is most likely?
A. IgA nephropathy (Berger disease)
B. Membranous nephropathy
C. Poststreptococcal GN
D. Alport syndrome
E. Goodpasture syndrome
Answer: A
Explanation: IgA nephropathy presents with episodic gross hematuria concurrent with mucosal infections; mesangial IgA deposition is diagnostic.
Which of the following best distinguishes nephrotic from nephritic syndrome?
A. Nephrotic: hematuria predominates; nephritic: massive proteinuria
B. Nephrotic: heavy proteinuria, hypoalbuminemia, hyperlipidemia; nephritic: hematuria, hypertension, azotemia, RBC casts
C. Nephrotic: RBC casts; nephritic: fatty casts
D. All glomerular diseases are nephrotic only
E. Neither affects serum albumin
Answer: B
Explanation: Classic distinguishing features: nephrotic syndrome = massive proteinuria, hypoalbuminemia, edema, hyperlipidemia; nephritic = hematuria, RBC casts, hypertension, azotemia.
Which of the following drugs increases calcium reabsorption in the kidney and is thus used for calcium-stone prevention?
A. Hydrochlorothiazide
B. Furosemide
C. Acetazolamide
D. Mannitol
E. Spironolactone
Answer: A
Explanation: Thiazide diuretics reduce urinary Ca²⁺ excretion and are used to prevent recurrent calcium stones.
Which of the following best describes the pathophysiology of nephrogenic diabetes insipidus caused by lithium?
A. Lithium inhibits ADH release from posterior pituitary
B. Lithium downregulates AQP2 channels in collecting duct principal cells causing resistance to ADH
C. Lithium increases ADH receptor sensitivity
D. Lithium acts as an ADH agonist leading to hyponatremia
E. Lithium reduces thirst
Answer: B
Explanation: Lithium is taken up into principal cells and disrupts signaling, reducing AQP2 expression and response to ADH → nephrogenic DI with polyuria and low urine osmolality.
Which renal pathology is characterized by “spike and dome” electron microscopy and associated with antibodies to PLA2R in primary form?
A. Membranous nephropathy
B. Minimal change disease
C. FSGS
D. Membranoproliferative GN
E. IgA nephropathy
Answer: A
Explanation: Membranous nephropathy demonstrates subepithelial immune complex deposition producing spike and dome appearance. Anti-PLA2R antibodies occur in primary membranous nephropathy.
A patient with hyperaldosteronism is treated with spironolactone. Which of the following lab changes will occur?
A. Hypokalemia worsens
B. Metabolic acidosis corrects to alkalosis
C. Serum potassium increases (hyperkalemia risk)
D. Increased sodium retention
E. Increased amiloride excretion
Answer: C
Explanation: Spironolactone antagonizes aldosterone leading to decreased K⁺ secretion → risk of hyperkalemia.
(Clinical vignette) A 65-year-old woman with chronic urinary tract infections has radiopaque staghorn calculi composed of magnesium ammonium phosphate. What organism is frequently implicated?
A. Proteus mirabilis (urease-producing)
B. E. coli (non-urease producing)
C. Staphylococcus aureus only
D. Candida albicans
E. Pseudomonas aeruginosa
Answer: A
Explanation: Struvite stones (staghorn calculi) are composed of magnesium ammonium phosphate, associated with urease-producing organisms such as Proteus, which alkalinize the urine.
Which of the following statements about renal glomerular filtration is true?
A. Only free plasma water is filtered, not proteins; filtration of a substance depends on size and charge; negatively charged molecules are repelled by GBM.
B. Large proteins like albumin are freely filtered.
C. Positively charged proteins are repelled by GBM more than negatively charged ones.
D. The slit diaphragm is permeable to cells.
E. Molecular charge does not affect filtration.
Answer: A
Explanation: Filtration is selective for size and charge: GBM has negative charges (heparan sulfate) that repel anionic proteins; albumin (large, negative) is mostly retained.
Which of the following is most likely to produce hyperkalemia?
A. Loop diuretics
B. Thiazide diuretics
C. ACE inhibitors
D. Beta-2 agonists
E. Insulin
Answer: C
Explanation: ACE inhibitors reduce aldosterone → decreased K⁺ excretion → hyperkalemia. Beta-2 agonists and insulin shift K⁺ into cells and lower serum K⁺.
Which of the following clinical features is typical of nephritic syndrome?
A. Edema, hyperlipidemia, oval fat bodies
B. Hematuria with RBC casts, oliguria, hypertension
C. Massive proteinuria (>3.5 g/day) only
D. Asymptomatic hematuria without protein loss
E. Kidney stones and hematuria with acid urine
Answer: B
Explanation: Nephritic syndrome classically has hematuria with RBC casts, oliguria, hypertension, and varying degrees of proteinuria (usually subnephrotic).
Which renal abnormality is associated with sickle cell disease?
A. Renal papillary necrosis due to sickling in vasa recta leading to hematuria and proteinuria
B. Membranous nephropathy
C. Goodpasture syndrome
D. Low GFR due to hyperfiltration only
E. Liddle syndrome
Answer: A
Explanation: Sickle cell disease predisposes to renal papillary necrosis (ischemia from sickling in vasa recta) causing hematuria, proteinuria, and possible concentration defect.
Which of the following best describes the effect of sympathetic activation on the kidney during hemorrhage?
A. Afferent arteriole dilation to increase GFR
B. Increased RBF and diuresis
C. Constriction of afferent arteriole via alpha-1 → decreased GFR and decreased urine output; increased renin via beta-1 on JG cells
D. Inhibition of RAAS
E. Decreased proximal reabsorption of sodium
Answer: C
Explanation: Sympathetic tone during hypovolemia causes afferent arteriole constriction → decreased RBF and GFR, increases proximal reabsorption and renin release (β1 stimulation of JG cells).
(Clinical vignette) A patient presents with sudden flank pain and gross hematuria. CT shows renal infarct due to thromboembolus from atrial fibrillation. Which portion of nephron is most susceptible to ischemic injury?
A. Renal cortex glomeruli only
B. Proximal tubule and thick ascending limb (high metabolic demand)
C. Collecting duct only
D. Thin descending limb only
E. Bowman’s capsule epithelium
Answer: B
Explanation: Proximal tubule and TAL have high metabolic activity and are most susceptible to ischemic injury (ATN). Cortex receives most blood but tubules are vulnerable.
Which of the following is an expected acid–base disturbance in salicylate (aspirin) overdose early on?
A. Pure metabolic acidosis only
B. Respiratory alkalosis due to stimulation of respiratory center; later combined with metabolic acidosis → mixed respiratory alkalosis + metabolic acidosis
C. Metabolic alkalosis only
D. Pure respiratory acidosis
E. No acid–base disturbance
Answer: B
Explanation: Early salicylate toxicity stimulates respiratory center → respiratory alkalosis; later metabolic acidosis develops (organic acids) → mixed picture.
Which of the following best describes the tubular maximum (Tm) for glucose?
A. It is the plasma concentration at which glucose first appears in urine
B. It is the maximum rate of glucose reabsorption; when filtered load exceeds Tm, glucosuria occurs
C. It is irrelevant to SGLT2 inhibitors
D. Tm increases in diabetes mellitus
E. Tm equals GFR × plasma glucose
Answer: B
Explanation: Tm is the maximum transport capacity of nephron for reabsorption; when filtered load (GFR × plasma glucose) > Tm, glucose appears in urine (threshold). SGLT2 inhibitors lower Tm.
Which of the following mechanisms leads to hyponatremia in SIADH?
A. Excess ADH → water retention → dilutional hyponatremia despite normal total body sodium
B. Low ADH → water diuresis
C. Primary hyperaldosteronism → hyponatremia
D. Excess aldosterone → increased water excretion
E. Increased GFR alone
Answer: A
Explanation: SIADH → inappropriate ADH secretion → water retention and dilutional hyponatremia with euvolemia. Urine osm is inappropriately high.
(Clinical vignette) A 55-year-old diabetic with CKD stage 4 has hyperphosphatemia and hypocalcemia. Which hormonal change is expected?
A. Decreased PTH due to high phosphate
B. Secondary hyperparathyroidism (elevated PTH) due to reduced 1α-hydroxylase activity and hypocalcemia
C. Increased calcitriol from kidneys
D. Decreased FGF23
E. Primary hypoparathyroidism
Answer: B
Explanation: CKD reduces renal 1α-hydroxylase → decreased calcitriol → hypocalcemia → secondary hyperparathyroidism; phosphate retention also stimulates PTH and FGF23.
Which of the following is most accurate regarding creatinine as a GFR marker?
A. Creatinine is secreted slightly by proximal tubule so creatinine clearance overestimates GFR modestly
B. Creatinine is reabsorbed in PCT making it poor marker
C. Creatinine is filtered and fully reabsorbed
D. Creatinine clearance underestimates RPF
E. Creatinine cannot be used clinically
Answer: A
Explanation: Endogenous creatinine clearance slightly overestimates true GFR because a small amount is secreted by proximal tubule.
Which transporter is responsible for ammonium secretion in proximal tubule?
A. NHE3 secreting H⁺ which then forms NH₄⁺ in lumen indirectly; NH₄⁺ can substitute for H⁺ on NKCC2 and be trapped
B. ENaC secretes NH₄⁺ directly
C. SGLT2 secretes NH₄⁺
D. H⁺/K⁺ ATPase secretes NH₄⁺
E. Pendrin secretes NH₄⁺
Answer: A
Explanation: Ammoniagenesis produces NH₄⁺; NH₄⁺ can be secreted into lumen, and in TAL it can substitute for K⁺ on NKCC2. NHE3 contributes to H⁺ secretion facilitating ammonium handling.
(Clinical vignette) A 32-year-old man with long-standing IV drug use presents with nephrotic syndrome and segmental sclerosis on biopsy, particularly in areas of scarring. Which is the likely diagnosis?
A. Focal segmental glomerulosclerosis (FSGS)
B. Membranous nephropathy
C. Minimal change disease
D. Poststreptococcal GN
E. Alport
Answer: A
Explanation: FSGS is associated with HIV, heroin, obesity, sickle cell, and IV drug use; presents with nephrotic syndrome and focal segmental sclerosis on biopsy.
Which of the following is true regarding renal handling of urea?
A. Urea is passively reabsorbed in the collecting duct in the presence of ADH via urea transporters, contributing to medullary osmolarity
B. Urea is actively secreted in PCT via ATPase
C. Urea is not filtered at the glomerulus
D. Urea is entirely reabsorbed and never excreted
E. Urea secretion is increased by thiazide diuretics
Answer: A
Explanation: Urea is filtered and partly reabsorbed in PCT and collecting duct (ADH increases urea transporter UT-A1 expression) contributing to medullary interstitial osmolarity and concentrating ability.
Which of the following causes hypophosphatemia and bone disease due to renal phosphate wasting?
A. Fanconi syndrome (proximal tubular dysfunction)
B. Hypoparathyroidism
C. Primary hyperparathyroidism (but that causes phosphate wasting too)
D. Both A and C
E. None cause phosphaturia
Answer: D
Explanation: Fanconi syndrome (proximal tubular dysfunction) → phosphate wasting. Primary hyperparathyroidism increases phosphate excretion via PTH. Both can cause hypophosphatemia and bone issues.
Which hormone increases Na⁺ reabsorption in principal cells by increasing ENaC and Na⁺/K⁺ ATPase activity?
A. Aldosterone
B. ANP
C. ADH
D. PTH
E. BNP
Answer: A
Explanation: Aldosterone upregulates ENaC and Na⁺/K⁺ ATPase → increased Na⁺ reabsorption and K⁺ secretion.
(Clinical vignette) A 40-year-old woman presents with hematuria and hearing loss; family history reveals similar findings. Genetic testing shows collagen IV mutation. Her renal biopsy is likely to show which feature?
A. Splitting and thinning of GBM on electron microscopy — Alport syndrome
B. Subepithelial immune complexes — membranous nephropathy
C. Podocyte effacement — minimal change
D. Mesangial IgA deposition — IgA nephropathy
E. Immune complex granular deposits — PSGN
Answer: A
Explanation: Alport syndrome due to collagen IV mutation causes irregular thinning and splitting of GBM on EM, hematuria, progressive renal failure, sensorineural deafness.
Which of the following statements about the macula densa is correct?
A. It senses renal perfusion pressure directly
B. It senses NaCl delivery in the distal tubule and modulates renin release via tubuloglomerular feedback
C. It secretes aldosterone in response to low sodium
D. It is located in the proximal tubule
E. It increases GFR when NaCl delivery is low by constricting afferent arteriole
Answer: B
Explanation: Macula densa cells in the distal tubule sense NaCl; low NaCl delivery triggers renin release (via paracrine signals) and afferent arteriole dilation to increase GFR via tubuloglomerular feedback.
Which of the following contributes to metabolic alkalosis in a patient receiving excessive loop diuretics?
A. Volume contraction (contraction alkalosis), increased aldosterone → increased H⁺ secretion
B. Direct HCO₃⁻ secretory loss in PCT
C. Decrease in CO₂ production
D. Increased urinary NH₄⁺ excretion only
E. Loop diuretics cause metabolic acidosis
Answer: A
Explanation: Loop diuretics cause volume contraction → increase RAAS and aldosterone → increased H⁺ secretion and K⁺ loss leading to metabolic alkalosis.
Which of the following is the principal buffer in the urine for H⁺ excretion (titratable acid)?
A. Phosphate (HPO₄²⁻/H₂PO₄⁻)
B. Bicarbonate
C. Albumin
D. Creatinine
E. Urea
Answer: A
Explanation: Titratable acidity refers principally to phosphate buffer system in urine; ammonia (NH₃/NH₄⁺) is another major urinary buffer for acid excretion.
(Clinical vignette) A 55-year-old man with long-term NSAID use presents with progressive CKD and biopsy shows interstitial fibrosis with tubular atrophy; which mechanism best explains NSAID-induced renal damage?
A. Inhibition of prostaglandin synthesis (vasodilatory in afferent arteriole) leading to decreased renal perfusion and ischemic injury; also AIN
B. Direct immune complex deposition in GBM
C. Enhances RAAS causing hyperfiltration injury only
D. Direct podocyte apoptosis causing minimal change disease only
E. Blocks ADH causing nephrogenic DI
Answer: A
Explanation: NSAIDs inhibit COX → decreased prostaglandins (PGE2, PGI2) which dilate afferent arteriole, leading to decreased RBF and ischemic injury; they can cause AIN and chronic interstitial nephritis.
Which of the following describes the major renal adaptive response to chronic metabolic acidosis?
A. Decreased ammoniagenesis
B. Increased renal ammoniagenesis and increased glutamine metabolism to produce new bicarbonate
C. No change in renal handling
D. Increased HCO₃⁻ excretion
E. Increased bicarbonate reabsorption only
Answer: B
Explanation: Chronic metabolic acidosis induces renal ammoniagenesis (from glutamine) producing NH₄⁺ excreted in urine and net generation of new HCO₃⁻ to help correct acidosis.
Which of the following best explains why loop diuretics are effective antihypertensives in low GFR patients more than thiazides?
A. Loop diuretics act on TAL which maintains efficacy even in low GFR; thiazides need higher GFR to reach site of action and have less effect when GFR low
B. Thiazides cause hyperkalemia in low GFR
C. Loops block ACE
D. Thiazides increase RAAS only
E. Loops increase GFR
Answer: A
Explanation: Thiazides work at DCT and require adequate delivery (and some GFR) for effect; loops act at TAL and remain effective in patients with reduced GFR.
(Clinical vignette) A 4-year-old child presents with sudden onset periorbital edema and proteinuria one week after a viral URI. Biopsy (if done) likely shows normal light microscopy but EM shows diffuse foot process effacement. Which disease?
A. Minimal change disease
B. FSGS
C. Membranous nephropathy
D. IgA nephropathy
E. Alport
Answer: A
Explanation: Minimal change disease often follows URI or immunization in children, causes nephrotic syndrome, normal LM, EM shows podocyte foot process effacement.
Which renal lab change is commonly seen in patients with rhabdomyolysis?
A. Increased urine myoglobin leading to dark urine and ATN; hyperkalemia, hyperphosphatemia, metabolic acidosis
B. Hypokalemia only
C. Alkaline urine preventing injury
D. Decreased creatinine kinase only
E. Increased HCO₃⁻
Answer: A
Explanation: Rhabdomyolysis → myoglobinuria can cause ATN; labs show hyperkalemia, hyperphosphatemia, elevated CK, metabolic acidosis.
Which metabolic disturbance would cause a right shift of the oxygen-hemoglobin dissociation curve and could occur with kidney disease?
A. Increased 2,3-BPG due to anemia of CKD → right shift
B. Decrease in H⁺ causing left shift
C. Hypothermia causing right shift
D. Decreased CO₂ causing right shift
E. Increased affinity due to methemoglobinemia only
Answer: A
Explanation: In CKD anemia and chronic hypoxia increase 2,3-BPG which shifts curve right facilitating O₂ unloading. (Note: hypothermia left shifts; increased CO₂ and H⁺ shift right.)
Which of the following is an effect of metabolic acidosis on potassium distribution?
A. H⁺ shifts into cells in exchange for K⁺ causing hypokalemia
B. H⁺ shifts into cells causing hyperkalemia in serum
C. H⁺ shifts out of cells (extracellular) and K⁺ moves into cells causing hyperkalemia — actual effect: acidosis tends to cause hyperkalemia by shifting K⁺ out of cells in exchange for H⁺
D. No effect on K⁺
E. Metabolic acidosis always causes hypokalemia
Answer: C
Explanation: In metabolic acidosis, H⁺ enters cells and K⁺ exits → hyperkalemia (though total body K⁺ may be depleted due to urinary losses).
(Clinical vignette) A 58-year-old man has acute oliguria, muddy brown casts, and a BUN:Cr ratio ~10. He was hypotensive after surgery. Diagnosis?
A. Acute tubular necrosis (ATN), intrinsic renal failure
B. Prerenal azotemia
C. Postrenal obstruction
D. Nephritic syndrome
E. Chronic kidney disease
Answer: A
Explanation: ATN features muddy brown granular casts, low BUN:Cr (~10–15), oliguria, often after ischemic insult (hypotension). Prerenal has BUN:Cr >20 and low urine Na.
Which of the following changes does chronic kidney disease (CKD) cause in bone mineral metabolism?
A. Reduced 1,25-(OH)₂D3 (calcitriol) → decreased Ca²⁺ absorption → hypocalcemia → secondary hyperparathyroidism and renal osteodystrophy
B. Increased calcitriol production
C. Hypophosphatemia only
D. Decreased PTH due to hypercalcemia
E. Increased vitamin D activation
Answer: A
Explanation: CKD reduces 1α-hydroxylase activity → low calcitriol → hypocalcemia and phosphate retention causing secondary hyperparathyroidism and bone disease.
Which of the following is most useful to differentiate prerenal azotemia from intrinsic renal failure (ATN)?
A. Fractional excretion of sodium (FeNa) — low (<1%) in prerenal, high (>2%) in ATN (unless diuretics used)
B. Serum K⁺ only
C. Hematuria only
D. BUN:Cr always normal
E. Urine pH only
Answer: A
Explanation: FeNa is helpful: in prerenal kidneys, sodium reabsorption is high so FeNa <1%; in ATN FeNa >2% due to tubular damage. Diuretics can confound FeNa.
(Clinical vignette) A 30-year-old man presents with severe acne treated with isotretinoin who now has hypercalcemia and polyuria. Isotretinoin can cause hypercalcemia by what mechanism affecting kidney?
A. Increased vitamin D activity leading to increased intestinal Ca²⁺ absorption, hypercalcemia which can cause nephrogenic DI and polyuria
B. Direct receptor antagonism causing hypocalcemia
C. Low PTH levels causing hypocalcemia
D. Enhanced renal Ca²⁺ wasting only
E. No effect on kidney or calcium
Answer: A
Explanation: Isotretinoin may increase vitamin D activity or sensitivity leading to hypercalcemia; hypercalcemia can cause nephrogenic DI with polyuria.
Which pathology is classically associated with a "tram-track" appearance on light microscopy and subendothelial immune complex deposits?
A. Membranoproliferative (mesangiocapillary) glomerulonephritis (MPGN)
B. Membranous nephropathy
C. Minimal change disease
D. FSGS
E. Alport
Answer: A
Explanation: MPGN shows GBM duplication ("tram-track") due to immune complex deposition and mesangial interposition; often associated with hepatitis C.
A patient has severe metabolic alkalosis due to hyperaldosteronism. Which urinary electrolyte pattern is most likely?
A. Low urinary chloride (if chloride-responsive) and high urinary bicarbonate
B. Low urinary sodium only
C. High urinary potassium and low urinary chloride; alkalosis is often chloride-sensitive vs chloride-resistant distinction — primary hyperaldosteronism is chloride-resistant metabolic alkalosis with high urinary chloride? For primary hyperaldosteronism, urinary chloride is usually high due to continued NaCl excretion; but in contraction alkalosis from vomiting urinary Cl⁻ low.
D. Increased urinary ammonium only
E. Hypocalciuria only
Answer: C (interpretation: primary hyperaldosteronism → high urinary Cl⁻ & Na⁺ with K⁺ wasting)
Explanation: Primary hyperaldosteronism causes Na⁺ retention but also increased distal Na⁺ delivery and K⁺/H⁺ secretion → hypokalemic metabolic alkalosis. Urinary chloride varies: in aldosterone excess, urinary chloride tends to be high because NaCl is being handled; contrast vomiting (chloride-responsive) shows low urinary chloride. This question is advanced — focus on K⁺ wasting and metabolic alkalosis in hyperaldosteronism.