Nephrology Practice Questions

Q: Which of the following statements is FALSE regarding type 2 renal tubular acidosis?

Urine pH > 5.5. ### Explanation **Type 2 Renal Tubular Acidosis (RTA)**, also known as **Proximal RTA**, is characterized by a defect in the proximal convoluted tubule’s (PCT) ability to reabsorb filtered bicarbonate ($HCO_3^-$). #### Why Option B is the Correct (False) Statement: In Type 2 RTA, although the proximal tubule fails to reabsorb bicarbonate initially, the distal tubule remains functional. Once the plasma bicarbonate level drops below the "renal threshold" (typically 12–20 mEq/L), the distal nephron is capable of acidifying the urine normally. Therefore, in a steady state of chronic acidemia, the **urine pH is typically 5.5 is a hallmark of **Type 1 (Distal) RTA**, where the distal tubule cannot secrete $H^+$ ions. #### Analysis of Incorrect Options: * **Option A (Proximal tubule defect):** This is true. The primary pathology is the loss of carbonic anhydrase activity or sodium-bicarbonate cotransporters in the PCT. * **Option C (Normal anion gap):** This is true. All RTAs are characterized by a **Normal Anion Gap Metabolic Acidosis (NAGMA)**, as the loss of $HCO_3^-$ is compensated by an increase in serum Chloride ($Cl^-$), leading to hyperchloremia. * **Option D (Fanconi syndrome present):** This is true. Type 2 RTA is frequently associated with generalized proximal tubule dysfunction (Fanconi Syndrome), leading to phosphaturia, glycosuria, aminoaciduria, and uricosuria. #### High-Yield Clinical Pearls for NEET-PG: * **Type 1 RTA (Distal):** Inability to secrete $H^+$; Urine pH > 5.5; associated with hypokalemia and **nephrolithiasis** (calcium phosphate stones). * **Type 2 RTA (Proximal):** Inability to reabsorb $HCO_3^-$; Urine pH < 5.5 (eventually); associated with **osteomalacia/rickets**. * **Type 4 RTA (Hyperkalemic):** Associated with **Aldosterone deficiency or resistance**; the only RTA with **high serum potassium**. * **Mnemonic:** "Bi-**P**-ar-**T**-ite" — **P**roximal is Type **2**.

Q: What electrolyte disturbance is seen in rhabdomyolysis?

Hyperphosphatemia. Rhabdomyolysis involves the rapid breakdown of skeletal muscle, leading to the release of intracellular contents into the systemic circulation. **Why Hyperphosphatemia is correct:** Phosphate is a major intracellular anion [1]. When muscle cell membranes (sarcolemma) are damaged, massive amounts of inorganic phosphorus are leaked into the extracellular fluid [1]. This is further exacerbated if the patient develops secondary Acute Kidney Injury (AKI) due to myoglobinuria, as the kidneys become unable to excrete the excess phosphate load. **Analysis of Incorrect Options:** * **Hyponatremia:** While fluid shifts can occur, hyponatremia is not a classic hallmark of rhabdomyolysis. Electrolyte disturbances are primarily driven by the release of *intracellular* ions. * **Hypokalemia:** This is incorrect; **Hyperkalemia** is the most life-threatening electrolyte disturbance in rhabdomyolysis. Potassium is the primary intracellular cation, and its release from necrotic muscle can lead to dangerous cardiac arrhythmias. * **Metabolic alkalosis:** Rhabdomyolysis typically causes a **High Anion Gap Metabolic Acidosis (HAGMA)** due to the release of organic acids (like lactic acid) and the accumulation of sulfates/phosphates during renal failure. **High-Yield Clinical Pearls for NEET-PG:** 1. **Hypocalcemia (Early Phase):** Occurs because calcium deposits into damaged muscle (dystrophic calcification) and binds with excess phosphate. 2. **Hypercalcemia (Late/Recovery Phase):** As muscle heals, the deposited calcium is remobilized back into the blood. 3. **Diagnosis:** The most sensitive marker is an elevated **Serum Creatine Kinase (CK/CPK)**, typically >5 times the upper limit of normal. 4. **Urine Findings:** Urine appears "tea-colored" or "cola-colored." Dipstick is positive for blood (due to myoglobin), but microscopy shows **no RBCs**.

Q: In Type II Renal Tubular Acidosis (RTA), what is the typical serum potassium level?

Low. **Explanation:** **Type II Renal Tubular Acidosis (Proximal RTA)** is characterized by a defect in the proximal tubule's ability to reabsorb filtered bicarbonate ($HCO_3^-$) [1]. This leads to significant bicarbonate wasting in the urine. **Why the correct answer is Low (Hypokalemia):** The primary mechanism for hypokalemia in Type II RTA is twofold: 1. **Increased Distal Delivery of Sodium Bicarbonate:** The failure of the proximal tubule to reabsorb $HCO_3^-$ leads to an increased load of non-reabsorbable anions (bicarbonate) reaching the distal tubule. To maintain electrical neutrality, sodium follows. 2. **Hyperaldosteronism:** The resulting volume depletion (due to osmotic diuresis from bicarbonate) activates the Renin-Angiotensin-Aldosterone System (RAAS) [1]. Aldosterone acts on the collecting duct to reabsorb sodium in exchange for potassium, leading to significant urinary potassium wasting. **Analysis of Incorrect Options:** * **B (Normal):** Potassium is rarely normal in untreated Type II RTA; the physiological response to bicarbonate wasting almost always drives levels down. * **C & D (Elevated levels):** Hyperkalemia is a hallmark of **Type IV RTA** (Hypoaldosteronism/Resistance), not Type II. Levels above 7 mEq/L are medical emergencies and are not characteristic of any RTA unless associated with acute renal failure. **NEET-PG High-Yield Pearls:** * **Type II RTA** is often associated with **Fanconi Syndrome** (phosphaturia, glycosuria, aminoaciduria). * **Urine pH:** Initially >5.5, but can become **<5.5** once the plasma bicarbonate level drops below the "renal threshold," allowing the distal tubule to acidify the urine normally [1]. * **Comparison:** Both Type I (Distal) and Type II (Proximal) RTA present with **hypokalemia**, whereas Type IV presents with **hyperkalemia**. * **Treatment Caution:** Giving bicarbonate to Type II RTA patients can actually worsen hypokalemia by increasing distal bicarbonate delivery.

Q: Which of the following statements about adult polycystic kidney disease is true?

Hematuria can occur. **Explanation:** **Autosomal Dominant Polycystic Kidney Disease (ADPKD)** is the most common inherited cystic kidney disease [1]. It is characterized by the progressive development of numerous cysts in the renal parenchyma, leading to kidney enlargement and eventual renal failure [1]. **Why Option C is Correct:** **Hematuria** is a common clinical presentation in ADPKD. It occurs due to the **rupture of a cyst** into the renal collecting system or as a result of associated nephrolithiasis (kidney stones). It can manifest as either microscopic or gross hematuria and is often accompanied by flank pain [1]. **Analysis of Incorrect Options:** * **Option A:** ADPKD is an **Autosomal Dominant** disorder (linked to *PKD1* on chromosome 16 or *PKD2* on chromosome 4) [1]. Autosomal Recessive PKD (ARPKD) is a distinct entity typically seen in infancy/childhood. * **Option B:** Erythropoietin (EPO) levels are usually **normal or elevated** in ADPKD. Unlike other causes of chronic kidney disease where EPO is deficient, the cysts in ADPKD can produce EPO locally, often maintaining hemoglobin levels despite declining renal function. * **Option D:** **Berry aneurysms** (Circle of Willis) are a classic extra-renal association of ADPKD, occurring in approximately 5-10% of patients. Subarachnoid hemorrhage is a major cause of morbidity. **NEET-PG High-Yield Pearls:** * **Most common extra-renal manifestation:** Hepatic cysts (usually asymptomatic). * **Cardiac association:** Mitral Valve Prolapse (MVP). * **Other associations:** Diverticulosis, pancreatic cysts, and seminal vesicle cysts. * **Diagnosis:** Ultrasonography is the primary screening tool (Ravine’s criteria). * **Treatment:** Tolvaptan (V2 receptor antagonist) is used to slow cyst progression.

Q: Which of the following is NOT a feature of Alport syndrome according to the FLINTER diagnostic criteria?

Cardiovascular changes. Alport Syndrome is a hereditary disorder of basement membranes caused by mutations in genes encoding the **Type IV collagen** alpha chains ($\alpha$3, $\alpha$4, or $\alpha$5) [1]. This leads to structural defects in the Glomerular Basement Membrane (GBM), cochlea, and eye. **Why Cardiovascular changes is the correct answer:** The **Flinter Criteria** (1989) were established to standardize the diagnosis of Alport Syndrome. The four classic criteria focus on the renal, auditory, and ocular manifestations. **Cardiovascular changes are not part of the Flinter criteria**, nor are they a primary feature of Alport syndrome. While some patients may develop hypertension secondary to chronic kidney disease (CKD), it is a complication rather than a diagnostic hallmark. **Analysis of Incorrect Options (Flinter Criteria components):** * **Positive family history (A):** A history of hematuria or progression to end-stage renal disease (ESRD) in male relatives is a core criterion. * **Typical changes in renal biopsy (B):** Electron microscopy (the gold standard) shows characteristic **"basket-weave" appearance** (thickening, thinning, and splitting of the GBM) [1]. * **High-tone sensorineural deafness (C):** Bilateral sensorineural hearing loss, typically affecting high frequencies, is a classic extra-renal manifestation. * *(Note: The fourth Flinter criterion is **Ocular lesions**, specifically anterior lenticonus or maculopathy).* [1] **High-Yield Facts for NEET-PG:** * **Inheritance:** Most common is **X-linked Dominant** (85%, COL4A5 mutation). * **Ocular Hallmark:** **Anterior Lenticonus** (pathognomonic) and "Dot-and-fleck" retinopathy. * **Diagnosis:** Diagnosis is now increasingly made via genetic testing or skin biopsy (looking for absence of $\alpha$5 chain). * **Clinical Presentation:** Persistent microscopic hematuria in childhood, progressing to proteinuria and ESRD by the 2nd–3rd decade in males.

Q: A 64-year-old woman with type 2 diabetes for 10 years presents with increasing fatigue, dyspnea, and pedal edema. On examination, her blood pressure is 165/90 mmHg, pulse is 90/min, JVP is 4 cm, heart sounds are normal, lungs are clear, and there is 3+ pedal edema. Her urinalysis is positive for 3 gm/L of protein and shows no casts or red blood cells. An abdominal ultrasound reveals normal size kidneys and no hydronephrosis. Which of the following renal diseases is the most likely diagnosis in this patient?

Glomerulosclerosis with mesangial thickening. ### Explanation **Correct Option: C. Glomerulosclerosis with mesangial thickening** The patient presents with a long-standing history of Type 2 Diabetes Mellitus (10 years), hypertension, and nephrotic-range proteinuria (3 gm/L) leading to edema. This classic triad in a diabetic patient strongly suggests **Diabetic Nephropathy (DN)**. [2] The hallmark histopathological changes of DN include: 1. **Diffuse Glomerulosclerosis:** The most common finding, characterized by **mesangial matrix expansion and thickening** of the glomerular basement membrane (GBM). [2] [4] 2. **Nodular Glomerulosclerosis (Kimmelstiel-Wilson lesions):** Pathognomonic for DN, though present in only 15-30% of cases. [2] 3. **Renal Size:** Unlike most chronic kidney diseases, kidneys in diabetic nephropathy are typically **normal or enlarged** in size due to hyperfiltration and hypertrophy, matching this patient's ultrasound findings. **Why Incorrect Options are Wrong:** * **A. Acute Glomerulonephritis:** Typically presents with hematuria (RBC casts) and "active" urinary sediment, which are absent here. [1] [3] * **B. Obstructive Uropathy:** Would show hydronephrosis on ultrasound and usually presents with flank pain or fluctuating urine output rather than isolated heavy proteinuria. * **D. Renal Infarction:** Presents with acute onset flank pain, hematuria, and LDH elevation; it does not cause chronic nephrotic-range proteinuria. **NEET-PG High-Yield Pearls:** * **Earliest Clinical Sign of DN:** Microalbuminuria (30–300 mg/day). [2] * **Earliest Histological Change:** Thickening of the Glomerular Basement Membrane (GBM). [2] * **Pathognomonic Lesion:** Kimmelstiel-Wilson (KW) nodules (Ovoid, hyaline, PAS-positive nodules in the periphery of the glomerulus). [2] * **Management:** ACE inhibitors or ARBs are the first-line treatment as they reduce intraglomerular pressure by dilating the efferent arteriole.

Q: A patient presents with hematuria for many days. Investigations reveal renal calculi, calcifications in the wall of the urinary bladder, and a small contracted bladder. What is the most probable cause?

Schistosomiasis. ### Explanation The clinical triad of **hematuria**, **bladder wall calcification**, and a **small contracted bladder** in the presence of renal calculi is a classic presentation of **Schistosomiasis** (specifically *Schistosoma haematobium*) [1]. #### Why Schistosomiasis is Correct? * **Pathogenesis:** The adult flukes reside in the perivesical venous plexus [1]. Eggs are deposited in the bladder wall, inducing a granulomatous reaction and chronic inflammation. * **Calcification:** As the eggs die, they undergo calcification. On imaging, this appears as a characteristic "fetal head" or linear calcification of the bladder wall. * **Contracted Bladder:** Chronic inflammation leads to extensive fibrosis, reducing bladder capacity and compliance (thimble bladder). * **Calculi:** Urinary stasis and the presence of calcified eggs acting as a nidus frequently lead to secondary stone formation [3]. #### Why Other Options are Incorrect? * **Tuberculosis (TB):** While TB causes a "thimble bladder" and hematuria, the calcification in TB typically involves the **renal parenchyma** (putty kidney) or ureters rather than the bladder wall itself [3]. * **Amyloidosis:** Can cause bladder thickening and hematuria [2], but diffuse bladder wall calcification is not a characteristic feature. * **Carcinoma of the Bladder:** While *S. haematobium* is a risk factor for **Squamous Cell Carcinoma**, the primary presentation of a tumor is a filling defect or mass rather than diffuse wall calcification and contraction. #### High-Yield Clinical Pearls for NEET-PG * **Vector:** *Bulinus* snail. * **Infective stage:** Cercaria (penetrates skin during swimming) [1]. * **Diagnostic feature:** Terminal spined eggs in urine. * **Malignancy Risk:** Strongly associated with **Squamous Cell Carcinoma** of the bladder (unlike the more common Transitional Cell Carcinoma). * **Drug of Choice:** Praziquantel.

Question 1

Which of the following statements is FALSE regarding type 2 renal tubular acidosis?

Accepted Answer

Urine pH > 5.5

Answer

Proximal tubule defect

Answer

Normal anion gap

Answer

Fanconi syndrome present

Question 2

What electrolyte disturbance is seen in rhabdomyolysis?

Accepted Answer

Hyperphosphatemia

Answer

Hyponatremia

Answer

Hypokalemia

Answer

Metabolic alkalosis

Question 3

In Type II Renal Tubular Acidosis (RTA), what is the typical serum potassium level?

Accepted Answer

Low

Answer

Normal

Answer

5.7 mEq/L

Answer

>7 mEq/L

Question 4

Which of the following statements about adult polycystic kidney disease is true?

Accepted Answer

Hematuria can occur

Answer

Autosomal recessive disorder

Answer

Low erythropoietin level

Answer

Berry aneurysms are not associated with polycystic kidney disease

Question 5

A patient with chronic kidney disease on haemodialysis complains of chest pain and back pain shortly after dialysis initiation. The symptoms resolve spontaneously with reassurance. What is the most likely cause of these symptoms?

Accepted Answer

Type B anaphylactoid reaction to the dialyser

Answer

Anxiety related to the dialysis procedure

Answer

Anaphylaxis to ethylene oxide used for sterilization

Answer

Febrile non-haemolytic transfusion reaction

Question 6

Which of the following is NOT a feature of Alport syndrome according to the FLINTER diagnostic criteria?

Accepted Answer

Cardiovascular changes

Answer

Positive family history

Answer

Typical changes in renal biopsy specimen

Answer

High tone sensorineural deafness

Question 7

A 64-year-old woman with type 2 diabetes for 10 years presents with increasing fatigue, dyspnea, and pedal edema. On examination, her blood pressure is 165/90 mmHg, pulse is 90/min, JVP is 4 cm, heart sounds are normal, lungs are clear, and there is 3+ pedal edema. Her urinalysis is positive for 3 gm/L of protein and shows no casts or red blood cells. An abdominal ultrasound reveals normal size kidneys and no hydronephrosis. Which of the following renal diseases is the most likely diagnosis in this patient?

Accepted Answer

Glomerulosclerosis with mesangial thickening

Answer

Acute glomerulonephritis

Answer

Obstructive uropathy

Answer

Renal infarction

Question 8

Which of the following represents the best method in diagnosing medullary cystic disease of the kidney?

Accepted Answer

Biopsy

Answer

Ultrasound

Answer

Nuclear scan

Answer

Urography

Question 9

A patient presents with hematuria for many days. Investigations reveal renal calculi, calcifications in the wall of the urinary bladder, and a small contracted bladder. What is the most probable cause?

Accepted Answer

Schistosomiasis

Answer

Amyloidosis

Answer

Tuberculosis

Answer

Carcinoma of the urinary bladder

Question 10

Nephrocalcinosis is a feature of which of the following conditions?

Accepted Answer

Pseudohypoparathyroidism

Answer

Primary hyperparathyroidism

Answer

Medullary sponge kidney

Answer

Vitamin D intoxication

Nephrology — MCQs

Nephrology — MCQs

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