Nephrology Practice Questions

Q: A 30 year old man presents to the emergency with complaints of muscle weakness, nausea, vomiting and fatigue. ECG showed tall peaked T waves, prolonged PR interval, wide QRS and absent P. which of the following drugs is not used in management?

Beta antagonist. Beta antagonist - The patient's symptoms (muscle weakness, nausea, vomiting, fatigue) and ECG findings (tall peaked T waves, prolonged PR interval, wide QRS, absent P waves) are classic signs of severe hyperkalemia. Beta-antagonists are not used in the management of hyperkalemia and can potentially worsen it by shifting potassium out of cells or interfering with renal potassium excretion. - While beta-antagonists may be used for other cardiac conditions, they are contraindicated or not indicated for the acute management of hyperkalemia. Insulin - Insulin (often given with glucose) is a cornerstone of hyperkalemia treatment as it drives potassium from the extracellular space back into the intracellular space by stimulating the Na-K ATPase pump [1]. - This rapid cellular shift helps to lower serum potassium levels and stabilize the cardiac membrane [1]. Calcium gluconate - Calcium gluconate does not lower serum potassium levels but is crucial for protecting the cardiac membrane from the effects of hyperkalemia [2]. - It works by antagonizing the membrane excitability caused by high potassium, indicated by the wide QRS and absent P waves [2]. Sodium bicarbonate - In patients with metabolic acidosis (which can exacerbate hyperkalemia by causing potassium to shift out of cells), sodium bicarbonate can be administered. - By correcting acidosis, it promotes the intracellular shift of potassium, thereby helping to lower serum potassium levels.

Q: A patient presented with edema, oliguria and frothy urine. He has no past history of similar complaints. On examination, his urine was positive for 3+ proteinuria, no RBCs/WBCs and no casts. His serum albumin was 2.5 gm/L and serum creatinine was 0.5 mg/dL. The most likely diagnosis is:

Minimal change disease. ***Minimal change disease*** - The classic presentation of **edema**, **oliguria**, and **frothy urine** (due to heavy proteinuria), along with **isolated proteinuria** (no RBCs/WBCs/casts) and **low serum albumin**, points to **nephrotic syndrome** [1]. **Minimal change disease** is the most common cause of nephrotic syndrome in children and a significant cause in adults, often presenting acutely without prior history [1]. - The **normal serum creatinine** (0.5 mg/dL) indicates preserved renal function, which is typical in early minimal change disease before significant complications arise [2]. *Interstitial nephritis* - This condition is characterized by **inflammation of the renal interstitium**, often leading to **acute kidney injury** with an elevation in serum creatinine. It's typically associated with a history of **drug exposure** or **systemic autoimmune diseases**. - Urinalysis usually reveals **white blood cells**, **eosinophils**, and sometimes **WBC casts**, which are absent in this patient. *Membranous nephropathy* - While it causes **nephrotic syndrome** with heavy proteinuria, it often presents more **insidiously** and is more common in older adults. - Urinalysis typically shows **microscopic hematuria** in a significant proportion of cases, secondary to glomerular injury, which is not noted here. *IgA nephropathy* - This is a common cause of **glomerulonephritis**, primarily characterized by **recurrent macroscopic or microscopic hematuria**, often following an upper respiratory or gastrointestinal infection. - While proteinuria can occur, it's typically **not in the nephrotic range** (3+ proteinuria suggests heavy proteinuria), and prominent edema is usually absent unless severe renal failure has developed.

Q: In case of PSGN complication commonly seen are all except :

Bleeding diathesis. ***Bleeding diathesis*** - **Post-streptococcal glomerulonephritis (PSGN)** typically does not cause **bleeding diathesis**. Bleeding diathesis is primarily associated with **liver disease**, **bone marrow suppression**, or certain genetic disorders, not directly with PSGN. - While severe kidney failure can indirectly affect coagulation, it's not a common or direct complication leading to **bleeding diathesis** in PSGN. *Hypertensive encephalopathy* - PSGN often leads to **fluid overload** and **renin-angiotensin system activation**, causing severe **hypertension** [1]. - Uncontrolled hypertension can result in **hypertensive encephalopathy**, characterized by headaches, seizures, and altered mental status. *Hyperkalemia* - Renal insufficiency, common in PSGN, impairs the kidneys' ability to excrete **potassium**. - This can lead to **hyperkalemia**, a life-threatening electrolyte imbalance that can cause cardiac arrhythmias. *LVF* - **Fluid overload** and severe **hypertension** in PSGN can overwhelm the heart's pumping capacity [1]. - This can precipitate **left ventricular failure (LVF)**, leading to symptoms like dyspnea and pulmonary edema.

Q: Steroid resistance nephrotic syndrome is defined as failure to achieve remission after:-

8 weeks of daily Corticosteroid therapy. 8 weeks of daily Corticosteroid therapy - **Steroid-resistant nephrotic syndrome** is precisely defined as the failure to achieve remission after a full 8-week course of daily oral corticosteroids. - Remission is typically characterized by urine protein excretion of less than 0.3 mg/day or a urine protein-to-creatinine ratio of less than 0.2 mg/mg for three consecutive days. 12 weeks of daily Corticosteroid therapy - This duration is **longer than the standard definition** for assessing steroid resistance in nephrotic syndrome. - After 8 weeks, if remission is not achieved, further management strategies are usually considered, rather than simply extending the initial steroid course. 4 weeks of daily Corticosteroid therapy - This period is **too short** to definitively classify a patient as having steroid-resistant nephrotic syndrome. - A 4-week course is often considered an initial trial, but many patients will respond to steroids with a slightly longer duration of treatment. 6 weeks of daily Corticosteroid therapy - While a significant duration of steroid therapy, **6 weeks is still considered insufficient** to declare steroid resistance. - The consensus guidelines for defining steroid resistance specify a minimum of 8 weeks of daily treatment due to variability in individual response times.

Q: A 70 year old male, known case of chronic renal failure suffers from a pathological fracture of Rt femur, the diagnosis is -

Secondary Hyperparathyroidism. ***Secondary Hyperparathyroidism*** - **Chronic renal failure** causes **hyperphosphatemia** and **decreased production of calcitriol (active vitamin D)**. - This leads to hypocalcemia, which stimulates the parathyroid glands to produce excessive **parathyroid hormone (PTH)**, resulting in bone demineralization and **pathological fractures** [2]. *Scurvy* - Caused by **vitamin C deficiency**, leading to impaired collagen synthesis and fragility of blood vessels. - While it can cause bone pain and potential for fractures in severe cases, it is not directly associated with **chronic renal failure** as a primary cause of pathological fracture. *Vitamin D Resistant rickets* - This is a genetic disorder (e.g., X-linked hypophosphatemia) characterized by impaired renal phosphate reabsorption and normal or elevated PTH levels. - While it causes bone demineralization, it is typically a **childhood-onset condition** [1] and not directly linked to **acquired chronic renal failure** in a 70-year-old male. *Primary Hyperparathyroidism* - Characterized by autonomous **overproduction of PTH** due to parathyroid gland adenoma or hyperplasia, leading to **hypercalcemia** and hypophosphatemia. - Unlike secondary hyperparathyroidism, which is a compensatory response to hypocalcemia in the context of renal failure, primary hyperparathyroidism is a direct parathyroid gland pathology.

Q: ANCA is most specific and sensitive marker for

Idiopathic crescentic glomerulonephritis. ***Idiopathic crescentic glomerulonephritis*** - **ANCA** (Anti-neutrophil cytoplasmic antibodies) are highly specific and sensitive for certain **pauci-immune necrotizing glomerulonephritides**, which often present as **idiopathic crescentic glomerulonephritis** [1]. - **Crescentic glomerulonephritis** without immune complex deposition (pauci-immune) is frequently associated with **ANCA-associated vasculitis**, making ANCA a crucial diagnostic marker [1]. *Membranoproliferative glomerulonephritis* - This condition is primarily characterized by alterations in glomerular basement membrane and mesangial cell proliferation, often associated with **immune complex deposition** or **complement dysregulation**, not typically ANCA. - While various types exist, **ANCA is not a primary diagnostic marker** for membranoproliferative glomerulonephritis. *Post streptococcal Glomerulonephritis* - This form of glomerulonephritis is triggered by a preceding **streptococcal infection** and is characterized by **immune complex deposition** in the glomeruli [1]. - It is diagnosed by evidence of infection (e.g., elevated ASO titers) and specific **complement activation profiles**, not ANCA [1]. *Focal segmental Glomerulosclerosis* - This primary glomerular disease is characterized by **segmental scarring of the glomeruli**, leading to proteinuria, and is often **idiopathic** or secondary to various causes like genetic mutations or viral infections [1]. - It is not an autoimmune vasculitis and is **not associated with ANCA**.

Q: Which of the following indicates radiograph contrast induced nephropathy?

Increased creatinine levels. ***Increased creatinine levels*** - **Contrast-induced nephropathy (CIN)** is defined as an abrupt increase in **serum creatinine** following the intravascular administration of contrast material [1]. - A typical increase is defined as an absolute increase in serum creatinine of at least 0.3 mg/dL (26.5 µmol/L) or a 50% relative increase from baseline within 48-72 hours. *Decreased urine output* - While a **decreased urine output** (oliguria) can be a symptom of acute kidney injury, it is not the primary diagnostic criterion for **contrast-induced nephropathy**. - The diagnosis of CIN relies more specifically on changes in **renal function markers** like creatinine, rather than just urine volume [1]. *Increased bilirubin* - **Increased bilirubin** levels typically indicate **liver dysfunction** or **hemolysis**, not necessarily kidney injury. - There is no direct causal link between contrast media administration and elevated bilirubin as a marker of acute kidney damage. *Decreased bilirubin* - **Decreased bilirubin** levels are not associated with any form of organ damage and generally hold no clinical significance. - This finding would not indicate **contrast-induced nephropathy** or any other common pathology.

Q: What is the diagnosis for this patient with end-stage renal disease who developed skin changes after an imaging procedure?

Nephrogenic systemic fibrosis. **Nephrogenic systemic fibrosis** * This condition is strongly associated with exposure to **gadolinium-based contrast agents** in patients with severe **renal insufficiency** or **end-stage renal disease (ESRD)**. * It presents with **skin thickening** and hardening, often involving the extremities and trunk, which can progress to joint contractures and immobility. *Porphyria cutanea tarda* * This is a **disorder of heme synthesis** characterized by **fragile skin**, **blistering**, and **hypertrichosis** in sun-exposed areas [1]. * While it can be associated with liver disease and sometimes seen in patients with ESRD, it is not directly linked to contrast media exposure [1]. *Calciphylaxis* * This severe and rare syndrome involves **vascular calcification** and **skin necrosis**, predominantly seen in patients with ESRD. * It typically presents as painful, violaceous skin lesions that progress to ulcers, and while connected to ESRD, it is not triggered by imaging procedures. *Actinic elastosis* * This condition refers to **degeneration of elastic tissue in the skin** due to chronic and excessive **sun exposure**. * It is characterized by thickened, wrinkled, and yellowed skin and is not related to kidney disease or contrast agent exposure.

Q: Five days after an uneventful cholecystectomy, an asymptomatic middle-aged woman is found to have a serum sodium level of 125 mEq/L. Which of the following is the most appropriate management strategy for this patient?

Restriction of free water. ***Restriction of free water*** - The patient has **mild asymptomatic hyponatremia** (125 mEq/L) developed post-operatively, likely due to increased ADH secretion causing **dilutional hyponatremia**. [1, 3] - **Restricting free water intake** gently corrects the sodium concentration by limiting further dilution, allowing the kidneys to excrete excess water. [1] *Administration of hypertonic saline solution* - This is typically reserved for **severe (Na < 120-125 mEq/L) or symptomatic hyponatremia** (e.g., seizures, altered mental status). - In this asymptomatic patient, rapid correction with hypertonic saline can lead to **osmotic demyelination syndrome**, a severe neurological complication. [1] *Hemodialysis* - Hemodialysis is an invasive procedure generally indicated for **severe, refractory hyponatremia** or when there are signs of **water intoxication with cerebral edema**, neither of which is present here. - It is an **overly aggressive treatment** for mild asymptomatic hyponatremia. *Plasma ultrafiltration* - This procedure removes plasma water and solutes and is primarily used in cases of **fluid overload with hyponatremia** (e.g., in heart failure or renal failure) when other diuretics are ineffective. - In an asymptomatic patient with mild hyponatremia, ultrafiltration is **unnecessary and carries risks** associated with invasive procedures.

Q: A 16-year-old boy presents with acute onset gross hematuria and loin pain following a recent upper respiratory tract infection. He also reports mild diarrhea. Peripheral smear examination is normal. There is no history of decreased urine output. Serum C3 levels are normal. Probable diagnosis is?

Berger's disease. ***Berger's disease*** - This presentation of **gross hematuria** and **loin pain** occurring *shortly after* an upper respiratory tract infection and mild diarrhea is highly characteristic of **IgA nephropathy** (Berger's disease) [1]. - The **normal C3 levels** help differentiate it from other conditions like PSGN, where C3 is typically low. *Post-streptococcal glomerulonephritis (PSGN)* - While PSGN can cause hematuria following an infection, it typically has a **longer latency period** (1-3 weeks after streptococcal infection) [1]. - A key distinguishing feature is **low serum C3 levels**, which are noted as normal in this case. *Microangiopathic hemolytic anemia* - This condition involves **microangiopathic hemolytic anemia**, **thrombocytopenia**, and sometimes renal failure. - The problem states a **normal peripheral smear**, ruling out the characteristic fragmented red blood cells seen in microangiopathic hemolytic anemia. *Hemolytic Uremic Syndrome (HUS)* - HUS is characterized by the triad of **microangiopathic hemolytic anemia**, **thrombocytopenia**, and **acute kidney injury**. - The presence of a **normal peripheral smear** and absence of thrombocytopenia (implied by lack of mention) make HUS unlikely.

Question 1

A 30 year old man presents to the emergency with complaints of muscle weakness, nausea, vomiting and fatigue. ECG showed tall peaked T waves, prolonged PR interval, wide QRS and absent P. which of the following drugs is not used in management?

Accepted Answer

Beta antagonist

Answer

Insulin

Answer

Calcium gluconate

Answer

Sodium bicarbonate

Question 2

A patient presented with edema, oliguria and frothy urine. He has no past history of similar complaints. On examination, his urine was positive for 3+ proteinuria, no RBCs/WBCs and no casts. His serum albumin was 2.5 gm/L and serum creatinine was 0.5 mg/dL. The most likely diagnosis is:

Accepted Answer

Minimal change disease

Answer

Interstitial nephritis

Answer

Membranous nephropathy

Answer

IgA nephropathy

Question 3

In case of PSGN complication commonly seen are all except :

Accepted Answer

Bleeding diathesis

Answer

Hypertensive encephalopathy

Answer

Hyperkalemia

Answer

LVF

Question 4

Steroid resistance nephrotic syndrome is defined as failure to achieve remission after:-

Accepted Answer

8 weeks of daily Corticosteroid therapy

Answer

12 weeks of daily Corticosteroid therapy

Answer

4 weeks of daily Corticosteroid therapy

Answer

6 weeks of daily Corticosteroid therapy

Question 5

A 70 year old male, known case of chronic renal failure suffers from a pathological fracture of Rt femur, the diagnosis is -

Accepted Answer

Secondary Hyperparathyroidism

Answer

Scurvy

Answer

Vitamin D Resistant rickets

Answer

Primary Hyperparathyroidism

Question 6

ANCA is most specific and sensitive marker for

Accepted Answer

Idiopathic crescentic glomerulonephritis

Answer

Membranoproliferative glomerulonephritis

Answer

Post streptococcal Glomerulonephritis

Answer

Focal segmental Glomerulosclerosis

Question 7

Which of the following indicates radiograph contrast induced nephropathy?

Accepted Answer

Increased creatinine levels

Answer

Decreased urine output

Answer

Increased bilirubin

Answer

Decreased bilirubin

Question 8

What is the diagnosis for this patient with end-stage renal disease who developed skin changes after an imaging procedure?

Accepted Answer

Nephrogenic systemic fibrosis

Answer

Porphyria cutanea tarda

Answer

Calciphylaxis

Answer

Actinic elastosis

Question 9

Five days after an uneventful cholecystectomy, an asymptomatic middle-aged woman is found to have a serum sodium level of 125 mEq/L. Which of the following is the most appropriate management strategy for this patient?

Accepted Answer

Restriction of free water

Answer

Administration of hypertonic saline solution

Answer

Hemodialysis

Answer

Plasma ultrafiltration

Question 10

A 16-year-old boy presents with acute onset gross hematuria and loin pain following a recent upper respiratory tract infection. He also reports mild diarrhea. Peripheral smear examination is normal. There is no history of decreased urine output. Serum C3 levels are normal. Probable diagnosis is?

Accepted Answer

Berger's disease

Answer

Post-streptococcal glomerulonephritis (PSGN)

Answer

Microangiopathic hemolytic anemia

Answer

Hemolytic Uremic Syndrome (HUS)

Nephrology — MCQs

Nephrology — MCQs

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