Nephrology Practice Questions

Q: The most common form of acute kidney injury is:

Prerenal azotemia. ***Prerenal azotemia*** - This is the most prevalent form of **acute kidney injury (AKI)**, accounting for approximately 50-60% of all cases [1]. - It results from **decreased renal perfusion**, leading to reduced glomerular filtration without direct damage to the kidney parenchyma [1]. *Acute tubular injury* - This is an **intrinsic form of AKI** characterized by damage to the renal tubules, often due to ischemia or nephrotoxins [1]. - While common, it is usually a consequence of prolonged or severe prerenal AKI, and thus not the *most* common initial cause [1]. *Acute interstitial nephritis* - This involves inflammation of the kidney's **interstitial tissue**, often triggered by **allergic reactions to medications** or infections [2]. - It represents a smaller percentage of AKI cases compared to prerenal causes. *Acute glomerular disease* - This form of AKI involves direct injury to the **glomeruli**, such as in glomerulonephritis [2]. - While serious, glomerular diseases are significantly less common as a cause of overall AKI compared to prerenal factors.

Q: A patient with chronic kidney disease is experiencing prolonged vomiting episodes. Given the patient's arterial blood gas (ABG) results showing a pH of 7.42, a pCO2 of 40 mmHg, and a bicarbonate level of 25 mmol/L, what is the most likely acid-base disturbance?

Metabolic acidosis and metabolic alkalosis. Metabolic acidosis and metabolic alkalosis - The ABG values of **pH 7.42**, **pCO2 40 mmHg**, and **bicarbonate 25 mmol/L** appear normal, but this patient has **chronic kidney disease (CKD)** which predisposes to **metabolic acidosis** [3], and **prolonged vomiting** which causes **metabolic alkalosis** [1]. - The normal pH, pCO2, and bicarbonate with concurrent severe metabolic acidosis and alkalosis suggest a **mixed acid-base disorder** where one disturbance is counteracting the other, resulting in a near-normal ABG [5]. Metabolic acidosis and respiratory acidosis - **Chronic kidney disease** can lead to **metabolic acidosis** [3], but prolonged **vomiting** typically causes **metabolic alkalosis**, not acidosis [1]. - There are no signs of **respiratory acidosis** (e.g., elevated pCO2) in the provided ABG results [4]. Metabolic acidosis and compensated respiratory alkalosis - While **CKD** can cause **metabolic acidosis**, prolonged **vomiting** would cause **metabolic alkalosis**, not induce a **respiratory alkalosis** [1]. - A compensated respiratory alkalosis would typically show a **lower pCO2** than 40 mmHg [2]. Normal ABG repo with normal electrolytes - Although the provided ABG values are within the normal range, the patient's underlying conditions of **chronic kidney disease** and **prolonged vomiting** are strong indicators of significant acid-base imbalances. - **CKD** inherently makes proper acid-base regulation difficult, and **vomiting** directly impacts electrolyte and acid-base balance, making a truly normal state unlikely [1][5].

Q: In a case of hematuria of glomerular origin, urine examination shows the presence of all of the following except:

Acanthocytes. ***Acanthocytes*** - Acanthocytes, or "spur cells," are **abnormally shaped red blood cells with thorny projections**. While they can be seen in some renal diseases (e.g., end-stage renal disease), their presence is **not a defining characteristic or a specific marker of glomerular hematuria**. [1] - Glomerular hematuria is primarily characterized by features indicating red blood cell passage through a damaged glomerular basement membrane. *Crenated red cells* - **Crenated red cells** appear shrunken with thorny or scalloped borders due to water loss in hypertonic urine. [1] - While they can be seen in a urine sample, their presence **does not specifically indicate a glomerular origin** of hematuria as they form due to osmotic changes in the urine environment, not passage through a damaged glomerulus. [1] *Dysmorphic red cells* - **Dysmorphic red cells** are red blood cells that have undergone structural changes, such as blebbing or budding, as they pass through the damaged glomerular basement membrane. - Their presence is a **strong indicator of glomerular hematuria**, suggesting that the blood originates from the kidney's filtering units. [1] *Red cell casts* - **Red cell casts** are cylindrical structures formed in the renal tubules, composed of red blood cells embedded in a protein (Tamm-Horsfall) matrix. - They are considered **pathognomonic for glomerular bleeding or acute glomerulonephritis**, as they can only form when red blood cells enter the tubules from the glomeruli. [1]

Q: All of the following statements about hyponatremia are true, except:

Pseudohyponatremia is associated with low plasma osmolality. ***Pseudohyponatremia is associated with low plasma osmolality*** - **Pseudohyponatremia** is an artifact caused by very high levels of plasma proteins or lipids, which interfere with the measurement of sodium. - In pseudohyponatremia, the actual measured **plasma osmolality** is normal because it is largely determined by the effective osmoles like sodium, glucose, and urea, which are not truly diluted in this condition [2]. *Hyponatremia associated with hyperglycemia has high plasma osmolality* - **Hyperglycemia** leads to an osmotic shift of water from the intracellular to the extracellular space, diluting serum sodium concentration. - Despite the diluted sodium, the high glucose levels contribute significantly to plasma osmolality, resulting in a **high plasma osmolality** [1]. *Hyponatremia associated with SIADH is normovolemic* - In **SIADH (Syndrome of Inappropriate Antidiuretic Hormone Secretion)**, there is excessive secretion of ADH, leading to increased water reabsorption in the kidneys. - This results in dilutional hyponatremia, and the body's **effective circulating volume** remains normal or slightly increased, classifying it as euvolemic or normovolemic hyponatremia [3]. *NSAIDs increase the potency of vasopressin* - **NSAIDs** can potentiate the action of **vasopressin (ADH)** by inhibiting prostaglandin synthesis in the kidneys [4]. - Prostaglandins normally antagonize ADH's effect on water reabsorption; therefore, their inhibition leads to increased water retention and can worsen or contribute to hyponatremia.

Q: ANCA is sensitive and specific for which condition?

ANCA-associated crescentic glomerulonephritis. ***ANCA-associated crescentic glomerulonephritis*** - **ANCA (Anti-neutrophil cytoplasmic antibodies)** are highly sensitive and specific for various **vasculitides** that often manifest as **rapidly progressive glomerulonephritis (RPGN)**, also known as crescentic glomerulonephritis [1]. - The presence of ANCA, particularly **p-ANCA (MPO-ANCA)** or **c-ANCA (PR3-ANCA)**, is a diagnostic hallmark of conditions like **granulomatosis with polyangiitis (Wegener's)**, **microscopic polyangiitis**, and **eosinophilic granulomatosis with polyangiitis (Churg-Strauss)**, all of which can cause crescentic glomerulonephritis [1]. *Post-streptococcal glomerulonephritis* - This condition is typically characterized by a **recent streptococcal infection** and is associated with **low C3 complement levels** and **anti-streptolysin O (ASO) titers**, not ANCA [2]. - Renal biopsy often shows **subepithelial humps** on electron microscopy and **C3 deposition**, which is distinct from ANCA-associated glomerulonephritis [2]. *Diffuse glomerulosclerosis* - This is a general term for widespread scarring of the glomeruli, which can result from various chronic conditions like **diabetes** or **hypertension**. - It is a morphological finding rather than a specific disease entity and is not directly associated with ANCA. *Henoch's Schönlein-Purpura* - This is an **IgA vasculitis** primarily affecting small vessels, characterized by a rash, arthralgia, abdominal pain, and kidney involvement (IgA nephropathy) [3]. - It is associated with **IgA deposits** in affected tissues, not ANCA [3].

Q: A 29-year-old male with HIV, on indinavir, zidovudine, and stavudine, presents with severe edema and a serum creatinine of 2.0 mg/dL. He has had bone pain for 5 years and takes large amounts of acetaminophen with codeine, aspirin, and ibuprofen. He is on prophylactic trimethoprim-sulfamethoxazole. Blood pressure is 170/110; urinalysis shows 4+ protein, 5 to 10 RBCs; 24-hour urine protein is 6.2 g. What is the most likely cause of his renal disease?

Focal sclerosis. Focal sclerosis - The combination of **HIV infection**, severe **proteinuria** (>3.5g/day, here 6.2g/day), and **hypertension** in an African American male strongly suggests **HIV-associated nephropathy (HIVAN)**, which often manifests as focal segmental glomerulosclerosis (FSGS) on biopsy [2]. - **HIVAN** is characterized by rapidly progressive renal failure, heavy proteinuria, and is more common in individuals of African descent [2]. *Indinavir toxicity* - **Indinavir** is a protease inhibitor known to cause **nephrolithiasis** (kidney stones) and **crystal-induced nephropathy**, presenting with acute kidney injury. - It typically does not cause the severe, sustained proteinuria seen in this patient, which is characteristic of glomerular disease [1]. *Analgesic nephropathy* - This condition is caused by chronic overuse of **NSAIDs and acetaminophen**, leading to **papillary necrosis** and **chronic interstitial nephritis**. - While the patient uses these medications, his primary presentation of heavy proteinuria and rapid decline in renal function points away from typical analgesic nephropathy, which usually involves milder proteinuria and sterile pyuria [1]. *Trimethoprim-sulfamethoxazole-induced interstitial nephritis* - هذا الدواء يمكن أن يسبب **التهاب الكلى الخلالي الحاد (AIN)**، والذي يترافق عادةً مع **حمى، طفح جلدي، فرط الحمضات (Eosinophilia)**، وارتفاع في الكرياتينين [1]. - While it can cause renal dysfunction, it is less likely to cause the severe proteinuria (6.2 g) observed in this patient, which is more indicative of a glomerular lesion [1].

Q: Which of the following conditions is associated with hyponatremia and decreased serum osmolality?

Irrigation of bladder after TURP. Irrigation of bladder after TURP - Transurethral resection of the prostate (TURP) syndrome can occur due to the systemic absorption of **hypotonic irrigation fluid** (e.g., glycine solution), leading to **dilutional hyponatremia** and decreased serum osmolality. [2], [4] - The absorbed fluid dilutes the extracellular fluid, causing a drop in **sodium concentration** and overall osmolality. [3] *Hyperlipidemia* - Severe hyperlipidemia can cause **pseudohyponatremia**, where the measured serum sodium is low but the true plasma sodium concentration is normal, due to an increased lipid volume displacing water. - This is an **artifact of measurement** and does not represent true hyponatremia with decreased serum osmolality; the plasma osmolality remains normal. *Hyperproteinemia* - Similar to hyperlipidemia, severe hyperproteinemia can lead to **pseudohyponatremia** by increasing the non-aqueous component of plasma, thus lowering the measured sodium concentration in a given volume of plasma. - This also does not cause a true decrease in **serum osmolality**. *CHF* - Congestive heart failure (CHF) can cause **hyponatremia** due to impaired water excretion, often driven by increased ADH (vasopressin) release. [1], [2] - However, the hyponatremia in CHF is typically **euvolemic or hypervolemic**, and while serum osmolality may be decreased, the primary mechanism is not direct influx of hypotonic fluid but rather impaired free water clearance secondary to systemic hemodynamics and hormonal factors. [2]

Q: An elderly hypertensive patient has diabetes mellitus and bilateral renal artery stenosis. The best management is:

Verapamil. ***Verapamil*** - **Verapamil**, a **calcium channel blocker**, is a suitable choice for this patient as it effectively lowers blood pressure without adversely affecting renal function in the presence of **bilateral renal artery stenosis**. - It also does not worsen **diabetes mellitus** or interfere with glucose metabolism, making it a safer option for this specific patient profile. *Enalapril* - **Enalapril**, an **ACE inhibitor**, is contraindicated in patients with **bilateral renal artery stenosis** because it can severely impair renal function and lead to acute kidney injury by reducing glomerular filtration pressure [1]. - While generally good for hypertension and diabetes, the presence of **bilateral renal artery stenosis** overrides these benefits due to the high risk of renal compromise [1], [2]. *Beta blockers* - **Beta blockers** can be used in hypertension, but they can **mask symptoms of hypoglycemia** in diabetic patients and may negatively affect lipid profiles and glucose control. - While not strictly contraindicated by renal artery stenosis, their potential metabolic side effects in a diabetic patient make them less ideal than **calcium channel blockers**. *Thiazides* - **Thiazide diuretics** can cause **glucose intolerance** and worsen glycemic control in patients with diabetes, which is a significant concern for this patient. - Although effective for hypertension, their use in patients with **renal artery stenosis** can sometimes lead to reduced renal blood flow due to volume depletion, potentially compromising kidney function.

Q: Which of these conditions is classified as a nephritic syndrome?

Post Infectious Glomerulonephritis. ***Post infectious Glomerulonephritis*** - Characterized by **hematuria, hypertension, and edema**, typically following an infection, such as streptococcal pharyngitis [2]. - Immune-mediated response leads to **decreased GFR** and signs of nephritic syndrome [1][2]. *Focal segmental glomerulosclerosis* - Primarily causes **nephrotic syndrome**, characterized by proteinuria and edema rather than hematuria [2]. - Often associated with **secondary causes** like obesity or HIV, not typically post-infectious. *Membranous Glomerulopathy* - Results in significant **proteinuria** and is classified as a **nephrotic syndrome** rather than a nephritic one [2][3]. - It presents with **edema and hypoalbuminemia**, lacking the hallmark features of hematuria. *Minimal change disease* - Predominantly causes **nephrotic syndrome** with heavy proteinuria and little to no hematuria [2]. - Young children are commonly affected, and it responds well to **corticosteroid therapy** [1].

Question 1

The most common form of acute kidney injury is:

Accepted Answer

Prerenal azotemia

Answer

Acute tubular injury

Answer

Acute interstitial nephritis

Answer

Acute glomerular disease

Question 2

A patient with chronic kidney disease is experiencing prolonged vomiting episodes. Given the patient's arterial blood gas (ABG) results showing a pH of 7.42, a pCO2 of 40 mmHg, and a bicarbonate level of 25 mmol/L, what is the most likely acid-base disturbance?

Accepted Answer

Metabolic acidosis and metabolic alkalosis

Answer

Metabolic acidosis and respiratory acidosis

Answer

Metabolic acidosis and compensated respiratory alkalosis

Answer

Normal ABG repo with normal electrolytes

Question 3

In a case of hematuria of glomerular origin, urine examination shows the presence of all of the following except:

Accepted Answer

Acanthocytes

Answer

Dysmorphic red cells

Answer

Crenated red cells

Answer

Red cell casts

Question 4

All of the following statements about hyponatremia are true, except:

Accepted Answer

Pseudohyponatremia is associated with low plasma osmolality

Answer

NSAIDs increase the potency of vasopressin

Answer

Hyponatremia associated with hyperglycemia has high plasma osmolality

Answer

Hyponatremia associated with SIADH is normovolemic

Question 5

ANCA is sensitive and specific for which condition?

Accepted Answer

ANCA-associated crescentic glomerulonephritis

Answer

Post streptococcal glomerulonephritis

Answer

Diffuse glomerulosclerosis

Answer

Henoch's Schönlein-Purpura

Question 6

A 29-year-old male with HIV, on indinavir, zidovudine, and stavudine, presents with severe edema and a serum creatinine of 2.0 mg/dL. He has had bone pain for 5 years and takes large amounts of acetaminophen with codeine, aspirin, and ibuprofen. He is on prophylactic trimethoprim-sulfamethoxazole. Blood pressure is 170/110; urinalysis shows 4+ protein, 5 to 10 RBCs; 24-hour urine protein is 6.2 g. What is the most likely cause of his renal disease?

Accepted Answer

Focal sclerosis

Answer

Analgesic nephropathy

Answer

Indinavir toxicity

Answer

Trimethoprim-sulfamethoxazole-induced interstitial nephritis

Question 7

Which of the following conditions is associated with hyponatremia and decreased serum osmolality?

Accepted Answer

Irrigation of bladder after TURP

Answer

Hyperproteinemia

Answer

CHF

Answer

Hyperlipedemia

Question 8

An elderly hypertensive patient has diabetes mellitus and bilateral renal artery stenosis. The best management is:

Accepted Answer

Verapamil

Answer

Enalapril

Answer

Beta blockers

Answer

Thiazides

Question 9

Which of the following factors contribute to anemia in chronic renal failure?

Accepted Answer

Multifactorial causes, including EPO deficiency, shortened RBC lifespan, and nutrient deficiencies

Answer

Erythropoietin (EPO) deficiency

Answer

Shortened red blood cell lifespan

Answer

Nutrient deficiencies (e.g., folate, iron)

Question 10

Which of these conditions is classified as a nephritic syndrome?

Accepted Answer

Post Infectious Glomerulonephritis

Answer

Minimal Change Disease

Answer

Membranous Glomerulopathy

Answer

Focal Segmental Glomerulosclerosis

Nephrology — MCQs

Nephrology — MCQs

On this page

Practice by Chapter

Want unlimited practice?