Nephrology Practice Questions

Q: A 22-year-old patient presents with hemoptysis and hematuria, and has basement membrane antibodies. What is the most likely diagnosis?

Goodpasture's syndrome. ### Explanation **Correct Option: B. Goodpasture's syndrome** Goodpasture’s syndrome is characterized by the clinical triad of **diffuse alveolar hemorrhage (hemoptysis)** and **glomerulonephritis (hematuria)**, mediated by **anti-glomerular basement membrane (anti-GBM) antibodies** [1], [2]. These antibodies are directed against the non-collagenous domain of the **alpha-3 chain of Type IV collagen**, which is found in both the glomerular and alveolar basement membranes. This leads to a Type II hypersensitivity reaction. On immunofluorescence, it classically shows a **linear deposition** of IgG along the basement membrane. **Why other options are incorrect:** * **A. Wegener’s Granulomatosis (GPA):** While it also presents with the pulmonary-renal syndrome (hemoptysis + hematuria), it is a small-vessel vasculitis associated with **c-ANCA (anti-PR3)**. It typically involves the upper respiratory tract (sinusitis, saddle nose deformity), which is absent here [2]. * **C. Polyarteritis Nodosa (PAN):** This is a medium-vessel vasculitis associated with Hepatitis B. It typically spares the lungs (no hemoptysis) and does not involve anti-GBM antibodies [2]. * **D. Churg-Strauss Syndrome (EGPA):** This is a small-vessel vasculitis characterized by **p-ANCA**, peripheral eosinophilia, and a strong history of asthma or allergic rhinitis [2]. **NEET-PG High-Yield Pearls:** * **Classic Triad:** Hemoptysis + Hematuria + Anti-GBM antibodies [1], [2]. * **Immunofluorescence:** Linear IgG pattern (Pathognomonic). * **Epidemiology:** Bimodal distribution (young men in their 20s and older women in their 60s). * **Treatment:** Plasmapheresis (to remove circulating antibodies) + Corticosteroids + Cyclophosphamide [1]. * **Key Distinction:** If only the kidney is involved (no lung hemorrhage), it is called **Anti-GBM Disease**; if both are involved, it is **Goodpasture’s Syndrome** [1], [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: Which of the following statements is FALSE about calciphylaxis?

It is typically associated with hypoparathyroidism.. ### Explanation **Calciphylaxis**, also known as **Calcific Uremic Arteriolopathy (CUA)**, is a rare but life-threatening syndrome characterized by systemic calcification of the tunica media of small-to-medium-sized dermo-hypodermal arteries. **Why Option D is the Correct Answer (False Statement):** Calciphylaxis is typically associated with **Secondary or Tertiary Hyperparathyroidism**, not hypoparathyroidism [1]. Elevated levels of Parathyroid Hormone (PTH), along with an elevated Calcium-Phosphate product (>55 mg²/dL²), promote the deposition of calcium in the vascular walls. Hyperparathyroidism drives the mineral bone disorder that leads to this extra-skeletal calcification [2]. **Analysis of Other Options:** * **Option A:** It is indeed a **calcific arteriopathy** most commonly seen in patients with End-Stage Renal Disease (ESRD) or Stage 4-5 **Chronic Kidney Disease (CKD)** [1]. * **Option B:** The clinical presentation often begins with **livedo reticularis** or violaceous plaques, which progress to extremely painful, necrotic, non-healing skin ulcers with an eschar. * **Option C:** **Vascular calcification** and intimal fibrosis leading to luminal narrowing and tissue ischemia are the hallmark histopathological features. **High-Yield Clinical Pearls for NEET-PG:** * **Risk Factors:** Female gender, obesity, diabetes mellitus, and use of **Warfarin** (which inhibits Matrix Gla Protein, a calcification inhibitor). * **Diagnosis:** Primarily clinical; however, a **skin biopsy** (deep punch) showing medial calcification and endovascular fibrosis is the gold standard. * **Management:** Multi-modal approach including wound care, lowering PTH, and the use of **Sodium Thiosulfate** (which helps dissolve calcium deposits). * **Prognosis:** Very poor, with high mortality rates usually due to secondary sepsis.

Q: Alport syndrome is associated with all except?

Peripheral retinal fleck. Explanation: Alport Syndrome is a hereditary disorder of basement membranes caused by mutations in the genes encoding the **alpha-3, alpha-4, or alpha-5 chains of type IV collagen**. This collagen is a crucial structural component of the glomerular basement membrane (GBM), the cochlea, and the eye [1]. **Why "Peripheral retinal fleck" is the correct answer:** The characteristic ocular finding in Alport syndrome is **Macular flecks** (perimacular retinopathy), which are yellowish-white spots around the fovea. These are typically asymptomatic and do not affect vision. **Peripheral** retinal flecks are more commonly associated with other conditions (like Benign Familial Fleck Retina) rather than the classic presentation of Alport Syndrome. **Analysis of other options:** * **Sensorineural deafness (A):** This is the most common extra-renal manifestation. It is bilateral and usually develops in late childhood or adolescence due to defects in the cochlear basement membrane. * **Posterior lenticonus (B):** This is a **pathognomonic** finding for Alport syndrome. It involves a conical protrusion of the posterior aspect of the lens into the vitreous chamber due to a weak lens capsule. * **Hematuria (D):** This is the earliest and most common clinical sign [1]. It typically presents as persistent microscopic hematuria, often with episodes of gross hematuria following upper respiratory infections. **NEET-PG High-Yield Pearls:** * **Inheritance:** Most common is **X-linked Dominant** (COL4A5 mutation). * **Electron Microscopy:** Shows a characteristic **"Basket-weave" appearance** (irregular thinning and thickening of the GBM) [1]. * **Clinical Triad:** Hereditary nephritis (hematuria/ESRD), sensorineural hearing loss, and ocular abnormalities (Posterior lenticonus). * **Leiomyomatosis:** Diffuse leiomyomatosis of the esophagus and tracheobronchial tree can be associated with certain X-linked deletions in Alport syndrome.

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: Clinical manifestations of acute glomerulonephritis include which of the following?

Hematuria and proteinuria. ### Explanation Acute Glomerulonephritis (AGN) is characterized by an inflammatory process within the renal glomeruli, leading to the classic **Nephritic Syndrome** [1]. **1. Why Hematuria and Proteinuria are correct:** The hallmark of AGN is glomerular capillary wall damage. This leads to increased permeability, allowing red blood cells and proteins to leak into the urine. * **Hematuria:** Often presents as "cola-colored" or smoky urine due to the presence of dysmorphic RBCs and RBC casts (pathognomonic for glomerular bleeding) [1], [3]. * **Proteinuria:** Usually in the sub-nephrotic range (<3.5 g/day), though it is a consistent finding due to the loss of the glomerular basement membrane's integrity [1]. **2. Analysis of Incorrect Options:** * **A. Chills and flank pain:** These are classic symptoms of **Acute Pyelonephritis** (upper urinary tract infection), not primary glomerular inflammation. * **B. Oliguria and generalized edema:** While these *can* occur in AGN (due to decreased GFR and salt/water retention), they are not as universally defining as the presence of blood and protein in the urine [1]. Generalized edema (anasarca) is more characteristic of Nephrotic Syndrome. * **C. Dysuria and hypotension:** Dysuria suggests a lower UTI (cystitis). AGN is typically associated with **hypertension** (due to fluid overload and renin activation), not hypotension [2]. * **Classic Triad of Nephritic Syndrome:** Hematuria, Hypertension, and Oliguria/Edema [1], [2]. * **Most common cause worldwide:** IgA Nephropathy (Berger’s disease) [2]. * **Post-Streptococcal GN (PSGN):** Occurs 1–3 weeks after a sore throat or skin infection; characterized by low C3 levels and "lumpy-bumpy" subepithelial humps on electron microscopy [1]. * **Red Cell Casts:** Their presence is the most specific indicator of a glomerular source of bleeding [3].

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.

Question 1

A 22-year-old patient presents with hemoptysis and hematuria, and has basement membrane antibodies. What is the most likely diagnosis?

Accepted Answer

Goodpasture's syndrome

Answer

Wagner's Granulomatosis

Answer

Polyarteritis Nodosa

Answer

Churg-Strauss syndrome

Question 2

What electrolyte disturbance is seen in rhabdomyolysis?

Accepted Answer

Hyperphosphatemia

Answer

Hyponatremia

Answer

Hypokalemia

Answer

Metabolic alkalosis

Question 3

Which of the following statements is FALSE about calciphylaxis?

Accepted Answer

It is typically associated with hypoparathyroidism.

Answer

It is a calcific arteriopathy seen in chronic kidney disease.

Answer

Livedo reticularis can be a clinical manifestation.

Answer

Vascular calcification is a characteristic feature.

Question 4

Which mode of vascular access for dialysis has the least chance of infection?

Accepted Answer

Arteriovenous fistula

Answer

Tunneled catheter

Answer

Venous catheter

Answer

Arteriovenous graft

Question 5

Alport syndrome is associated with all except?

Accepted Answer

Peripheral retinal fleck

Answer

Sensorineural deafness

Answer

Posterior lenticonus

Answer

Hematuria

Question 6

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 7

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 8

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 9

Clinical manifestations of acute glomerulonephritis include which of the following?

Accepted Answer

Hematuria and proteinuria

Answer

Chills and flank pain

Answer

Oliguria and generalized edema

Answer

Dysuria and hypotension

Question 10

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

Nephrology — MCQs

Nephrology — MCQs

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