Nephrology Practice Questions

Q: Which condition is characterized by hemoptysis, glomerulonephritis, and the presence of anti-glomerular basement membrane antibodies?

Goodpasture syndrome. ***Goodpasture syndrome*** - This condition is precisely defined by the triad of **hemoptysis** (due to pulmonary hemorrhage), rapidly progressive **glomerulonephritis**, and the presence of **anti-glomerular basement membrane (GBM) antibodies** [2], [4]. - The anti-GBM antibodies target collagen type IV in the basement membranes of the glomeruli and alveoli, leading to simultaneous lung and kidney damage [3], [4]. *Granulomatosis with polyangiitis (Wegener's granulomatosis)* - While it can cause **hemoptysis** and **glomerulonephritis**, it is primarily associated with **ANCA (anti-neutrophil cytoplasmic antibodies)**, specifically c-ANCA, not anti-GBM antibodies [2]. - It also commonly involves **upper and lower respiratory tract granulomatous inflammation**, which is not a defining feature in the prompt [4]. *Systemic lupus erythematosus (SLE)* - SLE can cause **glomerulonephritis** (lupus nephritis) and, less commonly, pulmonary hypertension and hemorrhage, but it is not typically associated with prominent **hemoptysis** as a primary presenting symptom in this context [1], [2]. - SLE is characterized by a wide range of autoimmune phenomena and the presence of **antinuclear antibodies (ANA)**, not anti-GBM antibodies. *Sarcoidosis* - Sarcoidosis is a multisystem **granulomatous disease** that most commonly affects the lungs (causing cough and dyspnea) and lymph nodes. - It sporadically causes **glomerulonephritis** but is not associated with **hemoptysis** or the presence of **anti-GBM antibodies**.

Q: A 40-year-old woman presents with facial swelling, periorbital edema, and proteinuria. Which condition is most likely responsible for her symptoms?

Nephrotic syndrome. ***Nephrotic syndrome*** - The combination of **facial swelling**, **periorbital edema**, and **proteinuria** is the classic triad of symptoms defining nephrotic syndrome [1]. - This syndrome is characterized by **massive proteinuria** (>3.5g/day), leading to **hypoalbuminemia**, which in turn causes reduced plasma oncotic pressure and fluid extravasation into interstitial spaces [1]. *Congestive heart failure* - While it can cause **edema**, it typically presents with **dependent edema** (e.g., in legs), **dyspnea**, and signs of fluid overload, not prominent facial or periorbital edema as a primary symptom with proteinuria. - **Proteinuria** can occur in chronic heart failure due to reduced renal perfusion, but it is usually not the massive proteinuria characteristic of nephrotic syndrome. *Liver cirrhosis* - Can cause **peripheral edema** and **ascites** due to portal hypertension and hypoalbuminemia, but **facial and periorbital edema** are less common as primary presenting symptoms. - While some **proteinuria** can be seen in chronic liver disease, it's typically milder and not the massive proteinuria seen in nephrotic syndrome. *Hypothyroidism* - Can cause **non-pitting edema** (myxedema), often described as puffy facial features and periorbital swelling, due to the accumulation of **hyaluronic acid** in the interstitial space. - However, **significant proteinuria** is not a characteristic feature of hypothyroidism; hence, it's less likely to explain the full constellation of symptoms.

Q: Which of the following factors most directly contributes to the development of edema in patients with nephrotic syndrome?

Hypoalbuminemia. Hypoalbuminemia - Nephrotic syndrome is defined by significant proteinuria leading to a decrease in serum albumin levels [2]. - Albumin is the primary protein responsible for maintaining oncotic pressure within the capillaries, and its deficiency (<3 g/dL) leads to fluid shifts from the intravascular space to the interstitial space, causing edema [1], [2]. Increased capillary permeability - While increased capillary permeability can cause edema, it is not the primary mechanism in nephrotic syndrome. - In nephrotic syndrome, the problem is loss of protein from the capillaries, rather than the capillaries themselves becoming excessively leaky to fluid in general. Hypertension - Hypertension can exacerbate edema by raising hydrostatic pressure, but it is not the initial or primary cause of edema in nephrotic syndrome [1]. - Edema in nephrotic syndrome can occur even in normotensive patients due to severe hypoalbuminemia [2]. Hypernatremia - Hypernatremia indicates high sodium levels in the blood, which would typically cause water to shift into the intravascular space, thus drawing fluid out of the interstitial space. - In actuality, patients with nephrotic syndrome often experience some degree of sodium retention, which contributes to fluid overload, but it is not the most direct cause of fluid moving from the capillaries into the interstitial tissue [3].

Q: A 58-year-old woman with chronic kidney disease has a serum potassium level of 5.8 mEq/L. What is the most likely cause?

Decreased renal excretion. ***Decreased renal excretion*** - **Chronic kidney disease (CKD)** is the most common cause of **hyperkalemia** due to the kidneys' reduced ability to excrete potassium [3]. - In CKD, the glomerular filtration rate (GFR) is significantly low, impairing the normal homeostatic mechanisms for potassium balance [3]. *Increased dietary potassium intake* - While excessive dietary potassium can contribute to hyperkalemia, it is usually not the sole cause in an individual with normal kidney function due to efficient renal excretion [1]. - In the context of CKD, even a moderate increase in dietary potassium can be problematic, but the primary underlying issue remains the impaired excretion. *Increased aldosterone secretion* - **Aldosterone** promotes potassium excretion in the kidneys; therefore, increased aldosterone secretion would typically lead to **hypokalemia**, not hyperkalemia [1]. - Conditions causing increased aldosterone (e.g., primary hyperaldosteronism) are known to cause potassium wasting [4]. *Hypercalcemia* - **Hypercalcemia** refers to elevated calcium levels in the blood and does not directly cause hyperkalemia. - Although it can cause cardiovascular and renal complications, it does not typically lead to a direct increase in potassium levels [2].

Q: What is the most common cause of acute kidney injury in hospitalized patients?

Acute tubular necrosis. ### Acute tubular necrosis - **Acute tubular necrosis (ATN)** is the most frequent cause of acute kidney injury (AKI) in hospitalized patients, often resulting from **ischemia** or **nephrotoxic drugs** [1]. - It involves direct injury to the **renal tubular epithelial cells**, leading to their dysfunction and subsequent decline in kidney function [1]. *Glomerulonephritis* - **Glomerulonephritis** is an inflammatory condition affecting the **glomeruli**, which are the filtering units of the kidney. - While it can cause AKI, it is a less common cause compared to ATN, and its presentation typically involves **hematuria** and **proteinuria** [1]. *Renal artery stenosis* - **Renal artery stenosis** primarily causes chronic kidney disease and **renovascular hypertension** due to reduced blood flow to the kidney. - Although severe, acute occlusion can cause AKI, it is not the most common cause of AKI in the general hospitalized population. *Drug-induced nephropathy* - **Drug-induced nephropathy** encompasses various forms of kidney damage caused by medications, including **acute interstitial nephritis** and direct tubular toxicity. - While a significant contributor to AKI, many cases of drug-induced AKI are specifically forms of ATN or allergic interstitial nephritis, making ATN a broader and more common category [1].

Q: Which of the following conditions is most commonly associated with high anion gap metabolic acidosis?

Diabetic ketoacidosis. ***Diabetic ketoacidosis*** - In **diabetic ketoacidosis (DKA)**, the body produces **ketoacids** (ketones) due to insulin deficiency, which are unmeasured anions causing a **high anion gap metabolic acidosis** [2]. - The accumulation of these organic acids lowers the **bicarbonate** level and pH, increasing the calculated anion gap. *Renal tubular acidosis* - **Renal tubular acidosis (RTA)** typically causes a **normal anion gap metabolic acidosis**, as the kidney's inability to excrete acid or reabsorb bicarbonate does not involve the accumulation of unmeasured anions [1]. - It results from specific defects in acid-base handling by the renal tubules, leading to hyperchloremic metabolic acidosis [1]. *Severe diarrhea* - Severe diarrhea causes **metabolic acidosis** due to the loss of **bicarbonate** in the stool. - This loss of bicarbonate without a corresponding increase in unmeasured anions results in a **normal anion gap (hyperchloremic) metabolic acidosis**. *Salicylate intoxication* - Salicylate intoxication is complex and often causes a **mixed acid-base disorder**, initially stimulating the respiratory center leading to **respiratory alkalosis** [1]. - As the intoxication progresses, it can cause **high anion gap metabolic acidosis** due to uncoupling of oxidative phosphorylation and impaired renal function, but DKA remains a more classic and distinct cause of solely high anion gap metabolic acidosis.

Q: What is the most effective treatment for reducing the progression of diabetic nephropathy?

Blood pressure control with ACE inhibitors. ***Blood pressure control with ACE inhibitors*** - **Angiotensin-converting enzyme (ACE) inhibitors** are crucial as they reduce intraglomerular pressure and proteinuria, thereby slowing the progression of **diabetic nephropathy** [1]. - Their nephroprotective effects go beyond blood pressure reduction, specifically targeting the **renin-angiotensin-aldosterone system (RAAS)** which is implicated in renal damage in diabetes [1]. *Optimal glycemic control* - While essential for overall diabetes management and preventing microvascular complications, **glycemic control** alone does not have as significant an impact on the progression of established diabetic nephropathy as RAAS blockade [1], [4]. - Its primary role is in **preventing the initial onset** and early stages of diabetic nephropathy rather than significantly reducing its progression once macroalbuminuria is present [2]. *High protein intake* - **High protein intake** can worsen diabetic nephropathy by increasing the glomerular filtration burden and contributing to hyperfiltration and kidney damage. - In patients with established diabetic nephropathy, a **low-protein diet** is often recommended to reduce renal workload and potentially slow disease progression. *Diuretic therapy* - **Diuretics** are used to manage volume overload and hypertension in patients with kidney disease but do not directly reduce the progression of diabetic nephropathy [3]. - They primarily alleviate symptoms and lower blood pressure through fluid removal, but they lack the specific **renal protective mechanisms** of ACE inhibitors [3].

Q: A 32-year-old man presents with acute kidney injury, hematuria, and red cell casts in the urine. He has a history of a recent upper respiratory tract infection. What is the most likely diagnosis?

IgA nephropathy. ***IgA nephropathy*** - This condition is characterized by episodes of **macroscopic hematuria** that typically occur concurrently with or shortly after an **upper respiratory tract infection**. [1] - The acute kidney injury, hematuria, and **red cell casts** in the urine are classic findings, with the timing of symptoms relative to the infection being a key differentiating factor. [1] *Post-infectious glomerulonephritis* - This typically presents with a **latency period** of one to three weeks after a streptococcal infection, not concurrently with it. [1] - While it can cause hematuria and acute kidney injury, the **timing of presentation** relative to the infection is different from IgA nephropathy. [1] *Goodpasture's syndrome* - This is an **autoimmune disease** affecting the kidneys and lungs, caused by antibodies against the glomerular basement membrane. - It usually presents with a combination of **pulmonary hemorrhage** and rapidly progressive glomerulonephritis, which are not mentioned here. *Lupus nephritis* - This is a kidney complication of **systemic lupus erythematosus (SLE)** and presents with a variety of patterns, often with non-specific symptoms. [2] - It is often associated with other systemic manifestations of SLE (e.g., **arthralgias, rash, serositis**), which are absent in this patient's presentation. [2]

Q: A patient who received a kidney transplant 2 years ago presents with progressive renal dysfunction and proteinuria. A biopsy shows interstitial fibrosis and tubular atrophy. What is the most likely cause of these findings?

Chronic rejection; adjust immunosuppressive therapy. ***Chronic rejection; adjust immunosuppressive therapy*** - Chronic rejection typically manifests with **progressive renal dysfunction** and **interstitial fibrosis** and is a common complication in kidney transplant recipients [1]. - This condition often requires **adjustment of immunosuppressive therapy** to control the ongoing immune response against the graft [1]. *Acute cellular rejection; increase corticosteroids* - Acute cellular rejection usually presents acutely within days to weeks post-transplant, unlike the chronic presentation described here. - While corticosteroids are used to manage acute rejection, they are not appropriate for chronic rejection management. *Recurrent glomerulonephritis; start plasmapheresis* - Recurrent glomerulonephritis would typically cause different histological findings and not the **interstitial fibrosis** seen in chronic rejection. - Plasmapheresis is indicated for specific conditions like **antibody-mediated rejection**, not typically for chronic rejection [2]. *Drug toxicity; discontinue nephrotoxic medications* - Drug toxicity may cause renal impairment, but the biopsy findings suggest **chronic rejection** rather than acute damage from medication [1]. - Discontinuing nephrotoxic medications may help, but it does not address the underlying issue of chronic rejection.

Q: A 60-year-old man presents with hematuria and flank pain. Laboratory results show elevated serum creatinine and red blood cell casts in the urine. What is the most likely diagnosis?

Glomerulonephritis. ***Glomerulonephritis*** - The presence of **hematuria**, **elevated serum creatinine**, and **red blood cell casts** in the urine is the classic triad indicating **glomerulonephritis**. - **Red blood cell casts** are pathognomonic for glomerular bleeding and inflammation. *Kidney stones* - Kidney stones typically present with **severe, colicky flank pain** and **hematuria**, but usually without elevated serum creatinine unless there's an obstruction. - While red blood cells may be present in the urine, **red blood cell casts** are not typically seen with kidney stones. *Pyelonephritis* - Characterized by **fever**, **flank pain**, and symptoms of a **urinary tract infection**, often with **white blood cell casts** in the urine analysis. - While leukocyturia is common, **red blood cell casts** are not a typical finding, and elevated creatinine is usually seen only in severe, complicated cases. *Interstitial nephritis* - Often presents with **fever**, **rash**, and **eosinophilia**, often due to an **allergic reaction** to drugs. - While it can cause elevated creatinine and sometimes hematuria, **white blood cell casts** (especially eosinophil casts) are more characteristic than red blood cell casts.

Question 1

Which condition is characterized by hemoptysis, glomerulonephritis, and the presence of anti-glomerular basement membrane antibodies?

Accepted Answer

Goodpasture syndrome

Answer

Granulomatosis with polyangiitis (Wegener's granulomatosis)

Answer

Systemic lupus erythematosus (SLE)

Answer

Sarcoidosis

Question 2

A 40-year-old woman presents with facial swelling, periorbital edema, and proteinuria. Which condition is most likely responsible for her symptoms?

Accepted Answer

Nephrotic syndrome

Answer

Congestive heart failure

Answer

Liver cirrhosis

Answer

Hypothyroidism

Question 3

Which of the following factors most directly contributes to the development of edema in patients with nephrotic syndrome?

Accepted Answer

Hypoalbuminemia

Answer

Increased capillary permeability

Answer

Hypertension

Answer

Hypernatremia

Question 4

A 58-year-old woman with chronic kidney disease has a serum potassium level of 5.8 mEq/L. What is the most likely cause?

Accepted Answer

Decreased renal excretion

Answer

Increased dietary potassium intake

Answer

Increased aldosterone secretion

Answer

Hypercalcemia

Question 5

What is the most common cause of acute kidney injury in hospitalized patients?

Accepted Answer

Acute tubular necrosis

Answer

Glomerulonephritis

Answer

Renal artery stenosis

Answer

Drug-induced nephropathy

Question 6

Which of the following conditions is most commonly associated with high anion gap metabolic acidosis?

Accepted Answer

Diabetic ketoacidosis

Answer

Renal tubular acidosis

Answer

Severe diarrhea

Answer

Salicylate intoxication

Question 7

What is the most effective treatment for reducing the progression of diabetic nephropathy?

Accepted Answer

Blood pressure control with ACE inhibitors

Answer

Diuretic therapy

Answer

Optimal glycemic control

Answer

High protein intake

Question 8

A 32-year-old man presents with acute kidney injury, hematuria, and red cell casts in the urine. He has a history of a recent upper respiratory tract infection. What is the most likely diagnosis?

Accepted Answer

IgA nephropathy

Answer

Post-infectious glomerulonephritis

Answer

Goodpasture's syndrome

Answer

Lupus nephritis

Question 9

A patient who received a kidney transplant 2 years ago presents with progressive renal dysfunction and proteinuria. A biopsy shows interstitial fibrosis and tubular atrophy. What is the most likely cause of these findings?

Accepted Answer

Chronic rejection; adjust immunosuppressive therapy

Answer

Acute cellular rejection; increase corticosteroids

Answer

Drug toxicity; discontinue nephrotoxic medications

Answer

Recurrent glomerulonephritis; start plasmapheresis

Question 10

A 60-year-old man presents with hematuria and flank pain. Laboratory results show elevated serum creatinine and red blood cell casts in the urine. What is the most likely diagnosis?

Accepted Answer

Glomerulonephritis

Answer

Kidney stones

Answer

Pyelonephritis

Answer

Interstitial nephritis

Nephrology — MCQs

Nephrology — MCQs

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