Nephrology Practice Questions

Q: Rhabdomyolysis is seen in all of the following conditions except?

Hyperphosphatemia. Rhabdomyolysis is a clinical syndrome involving the breakdown of skeletal muscle fibers with the release of intracellular contents (myoglobin, CPK, and electrolytes) into the circulation. **Why Hyperphosphatemia is the correct answer:** Hyperphosphatemia is a **consequence** of rhabdomyolysis, not a cause. When muscle cells lyse, they release large amounts of intracellular phosphate into the bloodstream. Other metabolic consequences include hyperkalemia, hyperuricemia, and hypocalcemia (initially). Therefore, while it is a hallmark finding in the lab results of a patient with rhabdomyolysis, it does not trigger the condition itself. **Analysis of other options (Causes of Rhabdomyolysis):** * **Prolonged seizure activity:** Excessive muscle hyperactivity leads to an imbalance between ATP demand and supply, resulting in muscle cell death. * **Severe hypothyroidism:** Myopathy is common in hypothyroidism. In severe cases (like Myxedema coma), it can progress to frank rhabdomyolysis due to impaired muscle metabolism and reduced mitochondrial activity. * **Myopathy:** Various underlying myopathies (inflammatory like polymyositis, or metabolic like McArdle disease) predispose the sarcolemma to injury, leading to rhabdomyolysis [1]. **NEET-PG High-Yield Pearls:** * **Triad:** Muscle pain, weakness, and dark (tea-colored) urine. * **Gold Standard Lab:** Serum Creatine Phosphokinase (CPK) levels >5 times the upper limit of normal. * **Renal Complication:** Acute Tubular Necrosis (ATN) caused by myoglobinuria. * **Urinalysis Clue:** Dipstick positive for blood but **microscopy negative** for RBCs (indicates myoglobinuria). * **Treatment Priority:** Aggressive IV fluid resuscitation to prevent Pigment-induced Acute Kidney Injury.

Q: Which gene is most commonly mutated in autosomal dominant polycystic kidney disease (ADPKD)?

PKD1. Explanation: Autosomal Dominant Polycystic Kidney Disease (ADPKD) is the most common inherited kidney disease [1]. It is characterized by the progressive development of numerous fluid-filled cysts in both kidneys, eventually leading to end-stage renal disease (ESRD). 1. Why PKD1 is correct: Approximately 85% of ADPKD cases are caused by mutations in the PKD1 gene, located on chromosome 16p13.3 [1]. This gene encodes the protein Polycystin-1, which is involved in cell-cell and cell-matrix interactions. Patients with PKD1 mutations typically present earlier and progress to ESRD at a younger age (mean age ~54 years) compared to PKD2 [1]. 2. Why other options are incorrect: * PKD2: Mutations in this gene (located on chromosome 4q21) account for the remaining ~15% of cases [1]. It encodes Polycystin-2. While clinically similar to PKD1, the disease course is generally milder and progresses to ESRD later in life (mean age ~74 years). * NPHS1: This gene encodes Nephrin and is mutated in Finnish-type Congenital Nephrotic Syndrome, not ADPKD. * HEF: This is not a recognized gene associated with polycystic kidney disease. High-Yield Clinical Pearls for NEET-PG: * Extra-renal manifestations: The most common is Liver cysts (Polycystic Liver Disease). The most serious is Berry aneurysms (Circle of Willis), which can lead to subarachnoid hemorrhage [1]. * Diagnosis: Ultrasonography is the primary screening tool; diagnostic criteria are based on the number of cysts relative to the patient's age [1]. * Treatment: Tolvaptan (a Vasopressin V2 receptor antagonist) is used to slow the progression of cyst growth and renal decline in high-risk patients. * Mnemonic: PKD1 is on Chromosome 16 (1+6=7; 16 is "sweet sixteen" and more common). PKD2 is on Chromosome 4.

Q: In which of the following conditions would the patient most likely be normotensive?

Bartter syndrome. **Explanation:** The correct answer is **Bartter syndrome**. This condition is a rare autosomal recessive renal tubular disorder characterized by defective salt reabsorption in the thick ascending limb of the loop of Henle. This leads to salt wasting, which triggers the Renin-Angiotensin-Aldosterone System (RAAS). While aldosterone levels are high (secondary hyperaldosteronism), the patient remains **normotensive or hypotensive** because the primary defect is volume depletion due to salt loss. **Analysis of Options:** * **Primary Hyperparathyroidism:** Approximately 20–40% of these patients have hypertension [1]. The mechanism is multifactorial, involving hypercalcemia-induced increase in peripheral vascular resistance and potential renal impairment. * **Hypothyroidism:** Often associated with **diastolic hypertension**. This occurs due to increased peripheral vascular resistance and low-turnover states despite a decrease in cardiac output. * **Cushing Syndrome:** Hypertension is present in over 80% of cases. It is caused by increased mineralocorticoid activity of cortisol, enhanced sensitivity to catecholamines, and activation of the RAAS. **High-Yield Clinical Pearls for NEET-PG:** * **Bartter vs. Gitelman:** Bartter syndrome presents early in life with polyuria and growth retardation (mimics Loop diuretics). Gitelman syndrome presents later with prominent hypomagnesemia and hypocalciuria (mimics Thiazides). * **Key Triad of Bartter:** Hypokalemia, Metabolic Alkalosis, and **Normotension** (despite high renin/aldosterone). * **Differential Diagnosis:** If a patient has hypokalemia, metabolic alkalosis, and **hypertension**, think of Conn’s syndrome (Primary Hyperaldosteronism) or Liddle syndrome.

Q: A 20-year-old male presents with features of acute renal failure 5 days after an episode of diarrhea. Blood examination shows thrombocytopenia and Hb 10 gm%. What is the likely cause?

Haemolytic uremic syndrome. ### Explanation The clinical presentation of **Acute Renal Failure (ARF)**, **Thrombocytopenia**, and **Anemia** (Microangiopathic Hemolytic Anemia) following a diarrheal episode is the classic triad of **Hemolytic Uremic Syndrome (HUS)**. **1. Why Option A is correct:** HUS is primarily caused by **Shiga toxin-producing *E. coli* (STEC)**, most commonly serotype **O157:H7**. The toxin causes endothelial injury in the glomerular microvasculature, leading to platelet aggregation (thrombocytopenia) and the formation of microthrombi. As Red Blood Cells (RBCs) pass through these narrowed vessels, they are mechanically shredded, resulting in **schistocytes** (fragmented cells) and hemolytic anemia. The renal involvement manifests as oliguria and azotemia. **2. Why the other options are incorrect:** * **B. Hereditary Spherocytosis:** This is a congenital membrane defect causing extravascular hemolysis in the spleen. It presents with jaundice and splenomegaly, not acute renal failure or thrombocytopenia. * **C. Hemolytic Crises:** While this involves rapid RBC destruction (often seen in G6PD deficiency or Sickle Cell Disease), it does not typically present with the specific triad of thrombocytopenia and prodromal diarrhea leading to ARF. * **D. Chronic Glomerulonephritis:** This presents with a long-term history of hypertension, proteinuria, and shrunken kidneys, rather than an acute onset following a gastrointestinal infection. **Clinical Pearls for NEET-PG:** * **Most common cause of ARF in children:** HUS. * **Peripheral Smear:** Look for **Schistocytes** (helmet cells). * **D+ HUS (Typical):** Associated with diarrhea (STEC). * **D- HUS (Atypical):** Associated with complement dysregulation (Factor H deficiency). * **Management:** Primarily supportive (dialysis, transfusion). **Antibiotics and anti-motility agents are contraindicated** as they may increase toxin release.

Q: Plasmapheresis is the treatment of choice for which of the following conditions?

Goodpasture's syndrome. **Explanation:** **Goodpasture’s Syndrome (Anti-GBM Disease)** is the correct answer because its pathogenesis involves circulating pathogenic autoantibodies directed against the alpha-3 chain of Type IV collagen in the glomerular and alveolar basement membranes [1]. **Plasmapheresis** is the treatment of choice because it directly and rapidly removes these circulating anti-GBM antibodies from the plasma, preventing further tissue damage [1]. It is typically combined with corticosteroids and cyclophosphamide to suppress further antibody production [1]. **Analysis of Incorrect Options:** * **Henoch-Schönlein Purpura (IgA Vasculitis):** This is usually a self-limiting condition, especially in children. Treatment is primarily supportive; steroids are used for severe abdominal or renal involvement, but plasmapheresis is not standard therapy. * **Wegener's Granulomatosis (GPA):** The mainstay of treatment is induction with corticosteroids and immunosuppressants (Cyclophosphamide or Rituximab). While plasmapheresis may be considered in severe cases with rapidly progressive glomerulonephritis (RPGN) or pulmonary hemorrhage, it is not the primary "treatment of choice." * **Acute Renal Transplant Rejection:** Cellular rejection is treated with high-dose steroids or anti-thymocyte globulin. Plasmapheresis is reserved only for antibody-mediated rejection (AMR), not all acute rejections. **High-Yield Clinical Pearls for NEET-PG:** * **Goodpasture’s Triad:** Glomerulonephritis (hematuria), Pulmonary hemorrhage (hemoptysis), and Anti-GBM antibodies. * **Immunofluorescence Pattern:** Characterized by **linear** IgG deposits along the glomerular basement membrane [1]. * **Other Indications for Plasmapheresis:** TTP (Treatment of choice), Guillain-Barré Syndrome, Myasthenia Gravis (crisis), and Hyperviscosity syndrome.

Q: At which stage of renal deterioration are the signs and symptoms of chronic renal failure (CRF) typically observed?

GFR 45 ml/min/1.73m 2. **Explanation:** Chronic Kidney Disease (CKD) is a progressive loss of renal function. The kidneys possess a significant **functional reserve**, meaning they can maintain homeostasis even when a large number of nephrons are lost [1]. 1. **Why Option C is Correct:** Clinical signs and symptoms of chronic renal failure (such as fatigue, anemia, nocturia, and mild electrolyte imbalances) typically do not manifest until the GFR falls below **50% of normal** (roughly <60 ml/min/1.73m²) [1]. Specifically, **Stage 3b CKD (GFR 30–44 ml/min/1.73m²)** is the threshold where metabolic changes become clinically evident. At a GFR of **45 ml/min**, the compensatory mechanisms of the remaining nephrons are overwhelmed, leading to the accumulation of nitrogenous waste (azotemia) and the onset of overt clinical symptoms [1]. 2. **Why Other Options are Incorrect:** * **Options A, B, and D (GFR 90, 80, and 70 ml/min):** These values represent Stage 1 or Stage 2 CKD. In these stages, patients are usually **asymptomatic**, as many diseases of the kidney are clinically silent in the early stages [1]. The remaining healthy nephrons undergo compensatory hypertrophy and hyperfiltration, maintaining normal excretory and endocrine functions. Diagnosis at these stages usually relies on markers of kidney damage (like albuminuria) rather than clinical symptoms. **High-Yield Clinical Pearls for NEET-PG:** * **Definition of CKD:** Evidence of kidney damage or GFR <60 ml/min/1.73m² for **≥3 months** [1]. * **First Clinical Sign:** Often **nocturia** (due to loss of concentrating ability) or **anemia** (due to decreased Erythropoietin) [1]. * **Most Common Cause:** Diabetes Mellitus (followed by Hypertension) [1]. * **Uremic Symptoms:** Usually appear when GFR drops below **15 ml/min** (Stage 5/ESRD), necessitating renal replacement therapy [1].

Q: What surgical procedure is most commonly associated with postoperative acute kidney injury?

Cardiac surgery with cardiopulmonary bypass. **Explanation:** **1. Why Cardiac Surgery is Correct:** Cardiac surgery involving **cardiopulmonary bypass (CPB)** is the most common surgical cause of postoperative Acute Kidney Injury (AKI). The pathophysiology is multifactorial: * **Ischemia-Reperfusion Injury:** Non-pulsatile blood flow during bypass can lead to renal hypoperfusion. * **Inflammatory Response:** Contact of blood with the bypass circuit triggers a systemic inflammatory response syndrome (SIRS). * **Hemolysis:** Mechanical trauma to RBCs releases free hemoglobin, which is nephrotoxic. * **Oxidative Stress:** Reintroduction of oxygenated blood leads to the formation of reactive oxygen species (ROS) that damage tubular cells. **2. Analysis of Incorrect Options:** * **Neurosurgery:** While prolonged procedures carry a risk of dehydration or SIADH/Diabetes Insipidus, they are not inherently associated with high rates of AKI compared to cardiac procedures. * **TURP:** This is more commonly associated with **TURP Syndrome** (dilutional hyponatremia due to absorption of glycine/irrigation fluid) rather than primary AKI. * **Carcinoma Breast Surgery:** This is typically a superficial/soft tissue surgery with minimal hemodynamic instability or fluid shifts, making the risk of AKI very low. **3. High-Yield Clinical Pearls for NEET-PG:** * **Definition:** Post-cardiac surgery AKI is defined as an increase in serum creatinine by ≥0.3 mg/dL within 48 hours. * **Risk Factors:** Pre-existing CKD, advanced age, prolonged bypass time (>120 mins), and use of intra-aortic balloon pump (IABP). * **Prevention:** Maintaining adequate mean arterial pressure (MAP) and avoiding nephrotoxic drugs (NSAIDs, ACE inhibitors) perioperatively are the primary preventive strategies. * **Prognosis:** Even a minor rise in creatinine post-cardiac surgery is independently associated with increased 30-day mortality.

Q: Restless leg syndrome (RLS) is commonly seen in which of the following conditions?

Chronic renal failure. **Explanation:** **Restless Leg Syndrome (RLS)**, also known as Willis-Ekbom Disease, is a common neurological complication of **Chronic Renal Failure (CRF)** [1], particularly in patients with End-Stage Renal Disease (ESRD) on hemodialysis. [2] **Why Chronic Renal Failure is Correct:** The exact pathophysiology in CRF is multifactorial but is primarily linked to **iron deficiency** (common in uremia) and **dopaminergic dysfunction**. Iron is a necessary cofactor for tyrosine hydroxylase, the rate-limiting enzyme in dopamine synthesis. Uremic toxins and the associated anemia in CRF exacerbate these symptoms. RLS in these patients typically presents as an irresistible urge to move the legs, often accompanied by uncomfortable sensations that worsen at rest and during the night. [1] **Analysis of Incorrect Options:** * **A, B, and D (Hypercalcemia, Hyperphosphatemia, Hyperkalemia):** While these electrolyte imbalances are frequent complications of Chronic Renal Failure, they do not directly cause RLS. * **Hypercalcemia** typically presents with "stones, bones, abdominal groans, and psychic moans." * **Hyperphosphatemia** contributes to secondary hyperparathyroidism and pruritus. * **Hyperkalemia** is a medical emergency primarily affecting cardiac conduction. **High-Yield Clinical Pearls for NEET-PG:** * **First-line treatment for RLS in non-uremic patients:** Dopamine agonists (e.g., Pramipexole, Ropinirole). * **Treatment in CRF:** Management involves improving dialysis adequacy, correcting iron deficiency (target ferritin >100 ng/mL), and using Gabapentin or Pregabalin (often preferred over dopamine agonists in uremic RLS). * **Secondary causes of RLS:** Iron deficiency anemia (most common), Pregnancy, Diabetes Mellitus (peripheral neuropathy), and CRF. [1]

Q: Which statement is true regarding post-streptococcal glomerulonephritis?

Renal biopsy is indicated in severe renal dysfunction.. Post-streptococcal glomerulonephritis (PSGN) is a classic nephritic syndrome following a skin (impetigo) or throat (pharyngitis) infection with Group A Beta-hemolytic Streptococcus [1]. **Why Option A is correct:** PSGN is typically a clinical diagnosis in children with a recent history of infection, hematuria, edema, and hypertension. A renal biopsy is **not** routinely required. However, it becomes mandatory if there is **severe renal dysfunction** (e.g., rapidly rising creatinine suggesting RPGN), atypical features (absence of latent period), or if the clinical course is prolonged (persistent low C3 beyond 8 weeks), to rule out other glomerular diseases like IgA nephropathy or Lupus nephritis [1]. **Why the other options are incorrect:** * **Option B:** While gross hematuria ("cola-colored urine") usually resolves within 1–2 weeks, **microscopic hematuria** can persist for up to **1 to 2 years** post-recovery. * **Option C:** PSGN is characterized by the activation of the alternative complement pathway [1]. Therefore, **Serum C3 levels are characteristically low** (hypocomplementemia) in >90% of patients during the acute phase, typically returning to normal within 6–8 weeks. * **Option D:** Elevated triglycerides are a hallmark of **Nephrotic Syndrome** (due to increased hepatic lipoprotein synthesis). PSGN is a **Nephritic Syndrome**, where lipid profiles are typically normal. **High-Yield Clinical Pearls for NEET-PG:** * **Latent Period:** 1–3 weeks after pharyngitis; 3–6 weeks after pyoderma. * **Light Microscopy:** "Starry sky" appearance or "Lumpy-bumpy" deposits [1]. * **Electron Microscopy:** Pathognomonic **subepithelial humps**. * **Immunofluorescence:** Granular deposits of IgG and C3. * **Prognosis:** Excellent in children (>95% complete recovery); more guarded in adults [1].

Question 1

In uremia, all of the following are reversed by dialysis except:

Accepted Answer

Sexual dysfunction

Answer

Pericarditis

Answer

Uremic lung

Answer

Neuropathy

Question 2

Rhabdomyolysis is seen in all of the following conditions except?

Accepted Answer

Hyperphosphatemia

Answer

Prolonged seizure activity

Answer

Severe hypothyroidism

Answer

Myopathy

Question 3

Which gene is most commonly mutated in autosomal dominant polycystic kidney disease (ADPKD)?

Accepted Answer

PKD1

Answer

PKD2

Answer

NHPS1

Answer

HEF

Question 4

In which of the following conditions would the patient most likely be normotensive?

Accepted Answer

Bartter syndrome

Answer

Primary hyperparathyroidism

Answer

Hypothyroidism

Answer

Cushing syndrome

Question 5

A 20-year-old male presents with features of acute renal failure 5 days after an episode of diarrhea. Blood examination shows thrombocytopenia and Hb 10 gm%. What is the likely cause?

Accepted Answer

Haemolytic uremic syndrome

Answer

Hereditary spherocytosis

Answer

Haemolytic crises

Answer

Chronic glomerulonephritis

Question 6

Plasmapheresis is the treatment of choice for which of the following conditions?

Accepted Answer

Goodpasture's syndrome

Answer

Henoch-Schönlein purpura

Answer

Wegener's granulomatosis

Answer

Acute renal transplant rejection

Question 7

At which stage of renal deterioration are the signs and symptoms of chronic renal failure (CRF) typically observed?

Accepted Answer

GFR 45 ml/min/1.73m
2

Answer

GFR 90 ml/min/1.73m
2

Answer

GFR 70 ml/min/1.73m
2

Answer

GFR 80 ml/min/1.73m
2

Question 8

What surgical procedure is most commonly associated with postoperative acute kidney injury?

Accepted Answer

Cardiac surgery with cardiopulmonary bypass

Answer

Neurosurgery

Answer

Transurethral resection of the prostate (TURP)

Answer

Carcinoma breast surgery

Question 9

Restless leg syndrome (RLS) is commonly seen in which of the following conditions?

Accepted Answer

Chronic renal failure

Answer

Hypercalcemia

Answer

Hyperphosphatemia

Answer

Hyperkalemia

Question 10

Which statement is true regarding post-streptococcal glomerulonephritis?

Accepted Answer

Renal biopsy is indicated in severe renal dysfunction.

Answer

Microscopic hematuria resolves within 2 weeks.

Answer

Serum C3 levels are normal.

Answer

Serum triglyceride levels are elevated.

Nephrology — MCQs

Nephrology — MCQs

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