Nephrology Practice Questions

Q: Acute anuria may occur in all of the following except:

Use of intravenous dextran in anemic patients. ***Use of intravenous dextran in anemic patients*** - **Dextran** is a plasma volume expander and does not directly cause renal failure or anuria in anemic patients. - While large amounts of dextran can rarely cause **osmotic nephrosis**, it's not typically associated with acute anuria, especially compared to the other options. *Acute pancreatitis* - Severe acute pancreatitis can lead to **prerenal acute kidney injury** due to **hypovolemia** from fluid sequestration and systemic inflammation [1]. - This can progress to **acute tubular necrosis** and anuria if not promptly managed [1]. *Performing intravenous urogram in patient with multiple myeloma* - Patients with **multiple myeloma** are highly susceptible to **contrast-induced nephropathy** due to their pre-existing renal damage from light chain deposition [1]. - This can severely worsen kidney function and lead to acute anuria [1]. *Use of furosemide in patients receiving cephalosporin* - The combination of **furosemide** (a loop diuretic) and **cephalosporins** (nephrotoxic antibiotics like cephaloridine) can cause **additive nephrotoxicity** [1]. - This interaction can lead to **acute kidney injury** and ultimately anuria, especially in susceptible individuals [1].

Q: Which of the following is the most effective treatment for severe acute hyperkalemia requiring definitive management?

Dialysis. ***Dialysis*** - **Hemodialysis** is the most effective and rapid method for definitively removing **potassium** from the body in cases of **severe acute hyperkalemia**, especially when other treatments are insufficient or renal function is compromised [2]. - It creates a **concentration gradient** that allows for efficient removal of excess potassium from the blood [2]. *Insulin and glucose* - This treatment promotes the **intracellular shift of potassium**, temporarily lowering serum potassium levels but does not remove potassium from the body. - While effective for acute management, it is not a definitive long-term solution as potassium can shift back out of cells. *Resin therapy* - **Potassium-binding resins** (e.g., sodium polystyrene sulfonate) exchange potassium for another ion (like sodium or calcium) primarily in the **gastrointestinal tract**, leading to potassium excretion. - These therapies work slowly and are generally not suitable for **severe acute hyperkalemia** requiring rapid definitive management. *Calcium gluconate* - **Calcium gluconate** is given to **stabilize the cardiac membrane** and reduce the risk of arrhythmias in hyperkalemia [1]. - It does not lower serum potassium levels but rather antagonizes its cardiac effects, making it an emergent symptomatic treatment, not a definitive potassium-lowering measure [1].

Q: Which of the following is not a contraindication for renal biopsy?

CRF with normal kidney. ***CRF with normal kidney*** - This is **not a contraindication** because chronic renal failure (CRF) with a normal-sized kidney often indicates a potentially **reversible or treatable** underlying kidney disease, making biopsy valuable for diagnosis and guiding treatment. [1] - A biopsy could help determine the specific cause of CRF, such as certain **glomerulonephropathies**, that might respond to targeted therapies. [1] *Bleeding diathesis* - A **bleeding diathesis**, such as severe **thrombocytopenia** or significant coagulopathy, significantly increases the risk of **hemorrhage** during and after a percutaneous renal biopsy. - This condition makes procedures that involve tissue penetration particularly hazardous due to uncontrolled bleeding. *60 % damage of kidney texture* - **Extensive kidney damage** (e.g., 60% damage or severely atrophic kidneys) often indicates **advanced, irreversible fibrosis**, where a biopsy is unlikely to provide therapeutically actionable information. [1] - The procedure carries risks, and if the kidney is severely compromised, the diagnostic yield is low, while the risk of complications (e.g., bleeding, infection) remains. *Uncontrolled hypertension* - **Uncontrolled hypertension** poses a significant risk for complications, particularly **post-biopsy bleeding** and **hematoma formation**, due to increased intravascular pressure. [1] - Blood pressure should be adequately controlled (e.g., below 140/90 mmHg) before performing a renal biopsy to minimize these vascular risks.

Q: Which of the following statements is most accurate regarding adult polycystic kidney disease (APKD)?

Autosomal dominant inheritance.. ***Autosomal dominant inheritance.*** - **Autosomal dominant polycystic kidney disease (ADPKD)** is the most common form, meaning only one copy of the mutated gene from one parent is sufficient to cause the disease [1]. - This inheritance pattern leads to a 50% chance of transmission to each child, which is characteristic of the adult form. *M/C cause of death is cardiovascular* - While **cardiovascular complications**, particularly **hypertension** and **heart failure**, are very common in ADPKD and contribute significantly to morbidity, the leading cause of death is **renal failure** requiring dialysis or transplantation [1]. - Many patients die from complications related to **end-stage renal disease (ESRD)**, such as **uremia** or complications from renal replacement therapy [1]. *Cysts can convert to cancer.* - While there is a slightly increased risk of **renal cell carcinoma** in ADPKD patients, the **cysts themselves do not typically transform into cancer**. - The malignancy usually arises from the normal kidney parenchyma between the cysts, not from malignant degeneration of the cyst lining. *PCKD associated with PKD2 gene is severe.* - Mutations in the **PKD2 gene** are generally associated with a **milder clinical course** and a later onset of end-stage renal disease (ESRD) compared to mutations in the **PKD1 gene** [1]. - Patients with **PKD1 mutations** typically experience a more severe disease, with a faster decline in renal function and earlier development of ESRD [1].

Q: At what glomerular filtration rate (GFR) is the term "end-stage renal disease (ESRD)" typically classified?

less than 15% of normal. ***Less than 15% of normal*** - **End-stage renal disease (ESRD)** is defined by a **glomerular filtration rate (GFR)** that falls below **15 mL/min/1.73 m²**, which is approximately **less than 15% of normal function**. - At this stage, **renal replacement therapy** (dialysis or transplantation) is typically required to sustain life. *15%—25% of normal* - This GFR range (15-25 mL/min/1.73 m²) corresponds to **Stage 4 chronic kidney disease (CKD)**, which is severe but not yet formally "end-stage." - Patients in this stage require careful monitoring and management, but may not immediately need renal replacement therapy. *10%—25% of normal* - This range overlaps with both **severe CKD (Stage 4)** and the beginning of **ESRD (Stage 5)**, but it is not the precise definition for ESRD. - The critical threshold for ESRD is uniformly established as GFR below 15 mL/min/1.73 m². *5%—10% of normal* - While a GFR in this range certainly indicates **ESRD**, the official classification includes any GFR **below 15% of normal** (or below 15 mL/min/1.73 m²), making "less than 15%" the most accurate and inclusive answer. - This smaller range describes a more advanced state within ESRD, but not the general definition.

Q: Increased anion gap metabolic acidosis is associated with all of the following conditions except:

Diarrhoea. ***Diarrhoea*** - Diarrhoea causes **non-anion gap metabolic acidosis** due to the loss of **bicarbonate-rich fluids** from the gastrointestinal tract [3]. - The anion gap remains normal because **chloride levels increase** to compensate for the bicarbonate loss, maintaining electroneutrality. *Starvation* - Prolonged starvation leads to **ketoacidosis** as the body breaks down fats for energy, producing **ketone bodies** (acetoacetate, beta-hydroxybutyrate) [1]. - These unmeasured anions increase the **anion gap**. *Salicylate poisoning* - Salicylate poisoning causes an **increased anion gap metabolic acidosis** because salicylates are organic acids and interfere with cellular metabolism [2]. - It often presents as a **mixed acid-base disorder** with an initial respiratory alkalosis due to central respiratory stimulation [2]. *Lactic acidosis* - Lactic acidosis results from the accumulation of **lactic acid**, an unmeasured anion, due to increased anaerobic metabolism (e.g., in shock or severe hypoxia) [2]. - This directly contributes to an **increased anion gap**.

Q: Which of the following is NOT a characteristic of Dent's disease?

Defect in limb of Loop of Henle. ***Defect in limb of Loop of Henle*** - Dent's disease is primarily a disorder affecting the **proximal renal tubule**, not the loop of Henle. - It is caused by mutations in the **CLC5 gene**, encoding a chloride channel, or in the OCRL1 gene. *Chloride channel defect* - Dent's disease is an X-linked recessive disorder caused by mutations in the **CLC5 gene**, which encodes a **chloride channel** located in the endosomes of the renal proximal tubule. - This channel's dysfunction leads to impaired protein reabsorption and other tubular defects. *Males are affected* - Dent's disease is an **X-linked recessive disorder**, meaning it predominantly affects males. - Females are typically carriers and are usually asymptomatic or have much milder symptoms due to random X-chromosome inactivation. *Nephrolithiasis* - Patients with Dent's disease frequently develop **nephrolithiasis (kidney stones)** due to hypercalciuria and hyperphosphaturia. - This is a common and often debilitating complication of the disease, contributing to progressive renal damage.

Q: Which of the following statements about acute tubular necrosis (ATN) is false?

Specific gravity of urine < 1.020 is true for ATN.. ***Specific gravity of urine < 1.020 is true for ATN.*** * This statement is false because a urine **specific gravity < 1.020** indicates **dilute urine**, which is characteristic of ATN due to the kidney's impaired concentrating ability. The question asks for the false statement, making this option the correct choice as it states a fact about ATN as being true. * In ATN, the damaged tubules cannot reabsorb water effectively, leading to fixed osmolality and low specific gravity, usually around **1.010 to 1.012**. *Urine sodium 20 mmol/L**. * Low urine sodium (< 20 mmol/L) is characteristic of **pre-renal azotemia**, where the kidneys are attempting to conserve sodium due to hypoperfusion [1]. *Blood urea: creatinine ratio 20:1** is typically seen in **pre-renal azotemia**, where there is disproportionate reabsorption of urea relative to creatinine [1]. *Urine Osmolality > 500 is true for ATN.* * This statement is false in the context of ATN; in ATN, the damaged renal tubules cannot concentrate urine, resulting in a **low urine osmolality**, typically ** 500 mOsm/kg** is characteristic of **pre-renal azotemia**, indicating intact tubular function striving to conserve water [1].

Q: Which of the following causes polyuria?

A.D.H insufficiency. ***A.D.H insufficiency*** - **Antidiuretic hormone (ADH)**, also known as **vasopressin**, regulates water reabsorption in the kidneys. Insufficiency leads to impaired reabsorption, resulting in excessive water excretion and thus **polyuria**. - This condition is characteristic of **diabetes insipidus**, where the kidneys cannot concentrate urine, leading to the production of large volumes of dilute urine, which is a key symptom. *Interstitial nephritis* - This condition involves **inflammation of the renal interstitium** and tubules, often leading to **acute kidney injury (AKI)** or chronic kidney disease. - While it can impair renal concentrating ability in some cases, it is not the primary or most direct cause of profound polyuria compared to ADH insufficiency. *Hypokalemia* - Severe **hypokalemia** (low potassium levels) can cause **nephrogenic diabetes insipidus**, leading to polyuria due to impaired renal response to ADH. - However, **hypokalemia itself is not the direct cause of polyuria**; rather, it induces a state in the kidney that mimics ADH resistance. *Rhabdomyolysis* - This involves the **breakdown of muscle tissue**, releasing contents like myoglobin into the bloodstream, which can damage the kidneys and cause **acute kidney injury (AKI)**. - AKI associated with rhabdomyolysis typically presents with **oliguria** (low urine output) or **anuria** (no urine output) due to tubular necrosis and obstruction, rather than polyuria.

Q: What is the most common initial presentation of Alport's syndrome?

Hematuria. ### Hematuria - This is the most consistent and often the earliest clinical manifestation of **Alport's syndrome**, appearing in nearly all affected individuals [1]. - **Microscopic hematuria** is typically present from childhood due to structural abnormalities in the **glomerular basement membrane (GBM)** [1]. ### Lenticonus - While **lenticonus** (conical protrusion of the lens) is a characteristic ocular manifestation of Alport's syndrome, it is not an initial or common presentation. - It usually develops later in life and is not a universal finding, unlike hematuria. ### AR inheritance - This option describes an **inheritance pattern** (autosomal recessive) and not a clinical presentation. - The most common inheritance pattern for Alport's syndrome is **X-linked (COL4A5 gene)**, affecting males more severely. ### End-stage renal disease - **End-stage renal disease (ESRD)** is a serious complication and the natural progression of Alport's syndrome, but it is not the initial presentation. - ESRD typically develops in late adolescence or early adulthood, following years of progressive renal damage [2].

Question 1

Acute anuria may occur in all of the following except:

Accepted Answer

Use of intravenous dextran in anemic patients

Answer

Use of furosemide in patients receiving cephalosporin

Answer

Acute pancreatitis

Answer

Performing intravenous urogram in patient with multiple myeloma

Question 2

Which of the following is the most effective treatment for severe acute hyperkalemia requiring definitive management?

Accepted Answer

Dialysis

Answer

Insulin and glucose

Answer

Resin therapy

Answer

Calcium gluconate

Question 3

Which of the following is not a contraindication for renal biopsy?

Accepted Answer

CRF with normal kidney

Answer

Bleeding diathesis

Answer

60 % damage of kidney texture

Answer

Uncontrolled hypertension

Question 4

Which of the following statements is most accurate regarding adult polycystic kidney disease (APKD)?

Accepted Answer

Autosomal dominant inheritance.

Answer

M/C cause of death is cardiovascular

Answer

PCKD associated with PKD2 gene is severe.

Answer

Cysts can convert to cancer.

Question 5

At what glomerular filtration rate (GFR) is the term "end-stage renal disease (ESRD)" typically classified?

Accepted Answer

less than 15% of normal

Answer

10%—25% of normal

Answer

15%—25% of normal

Answer

5%—10% of normal

Question 6

Increased anion gap metabolic acidosis is associated with all of the following conditions except:

Accepted Answer

Diarrhoea

Answer

Starvation

Answer

Lactic acidosis

Answer

Salicylate poisoning

Question 7

Which of the following is NOT a characteristic of Dent's disease?

Accepted Answer

Defect in limb of Loop of Henle

Answer

Chloride channel defect

Answer

Males are affected

Answer

Nephrolithiasis

Question 8

Which of the following statements about acute tubular necrosis (ATN) is false?

Accepted Answer

Specific gravity of urine < 1.020 is true for ATN.

Answer

Urine sodium < 20mmol/l is true for ATN.

Answer

Blood urea: creatinine ratio < 20 is true for ATN.

Answer

Urine Osmolality > 500 is true for ATN.

Question 9

Which of the following causes polyuria?

Accepted Answer

A.D.H insufficiency

Answer

Rhabdomyolysis

Answer

Interstitial nephritis

Answer

Hypokalemia

Question 10

What is the most common initial presentation of Alport's syndrome?

Accepted Answer

Hematuria

Answer

AR inheritance

Answer

End-stage renal disease

Answer

Lenticonus

Nephrology — MCQs

Nephrology — MCQs

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