Renal – 2017

✅ Dialysis
Dialysis clears creatinine from the blood, lowering serum creatinine rather than raising it.

Serum creatinine reflects the balance between its production (from muscle metabolism) and its excretion (mainly via glomerular filtration).

• Conditions that reduce renal perfusion (e.g., shock, dehydration, congestive heart failure) → decrease GFR → creatinine accumulates.

• Intense exercise transiently raises creatinine due to increased muscle metabolism.

• Dialysis, however, is used specifically to remove creatinine and urea from the blood in renal failure patients, thereby lowering serum levels.

Explanation of the Incorrect Options

❌ Congestive heart failure
Leads to reduced renal perfusion (prerenal azotemia) → ↑ creatinine.

❌ Intense exercise
Increases muscle breakdown and creatinine production → transient rise.

❌ Dehydration
Reduces effective circulating volume → ↓ GFR → ↑ creatinine.

❌ Shock
Severe hypoperfusion → acute kidney injury → marked rise in creatinine.

❌ Dialysis
Opposite effect — it reduces creatinine levels.

✅ Spironolactone
Spironolactone is a potassium-sparing diuretic that antagonizes aldosterone, leading to reduced potassium excretion and risk of hyperkalemia.

Mechanism:

• Spironolactone blocks aldosterone receptors in the distal nephron (late distal tubule & collecting duct).

• Normally, aldosterone increases Na⁺ reabsorption and K⁺ secretion.

• By antagonizing this action, spironolactone reduces Na⁺ reabsorption while retaining K⁺, which can lead to hyperkalemia.

This is a clinically important adverse effect, especially in patients with renal impairment or those taking ACE inhibitors/ARBs.

Explanation of the Incorrect Options

❌ Hydrocortisone
A glucocorticoid with mineralocorticoid activity; it promotes sodium retention and potassium loss → hypokalemia, not hyperkalemia.

❌ Acetazolamide
A carbonic anhydrase inhibitor; increases bicarbonate and potassium excretion → can cause hypokalemia.

❌ Furosemide
A loop diuretic; enhances Na⁺, K⁺, and water excretion → commonly leads to hypokalemia.

❌ Thiazides
Increase Na⁺ and K⁺ excretion in the distal tubule → also predispose to hypokalemia.

✅ Creation of arteriovenous fistula
An AV fistula provides durable vascular access with high blood flow for hemodialysis.

For hemodialysis, a patient requires a vascular access that can:

• Provide high blood flow (200–400 mL/min).

• Be long-lasting with low infection risk.

• Withstand repeated needle punctures.

The arteriovenous (AV) fistula, usually created surgically between the radial artery and cephalic vein at the wrist, is the gold standard. Over weeks, the vein becomes arterialized (thick-walled, high flow), making it suitable for dialysis needles.

Alternative access methods include AV grafts or central venous catheters, but these have higher complication rates compared to fistulas.

Explanation of the Incorrect Options

❌ Ventriculogallbladder shunt
Not a recognized procedure in nephrology; irrelevant here.

❌ Ventriculoperitoneal shunt
Used to treat hydrocephalus by draining CSF into the peritoneal cavity.

❌ Ventriculoatrial shunt
Also used in hydrocephalus; drains CSF into the right atrium.

❌ Lumboperitoneal shunt
CSF diversion procedure from lumbar subarachnoid space to peritoneum, not for dialysis.

✅ Hematuria
Nephritic syndrome is characterized by inflammation of the glomeruli, leading to leakage of red blood cells into the urine.

Nephritic syndrome results from glomerular inflammation (e.g., post-streptococcal glomerulonephritis, lupus nephritis). Its classic features are:

• Hematuria (often microscopic or gross, with RBC casts).

• Mild to moderate proteinuria (not massive, < 3.5 g/day).

• Hypertension (due to fluid retention).

• Azotemia (reduced GFR).

• Oliguria (reduced urine output).

By contrast, nephrotic syndrome is marked by massive proteinuria, hypoalbuminemia, edema, and lipiduria.

Explanation of the Incorrect Options

❌ Hypoalbuminemia
Seen in nephrotic syndrome, due to heavy protein loss, not typically in nephritic syndrome.

❌ Proteinuria
Mild proteinuria is present, but it is not the defining feature (massive proteinuria defines nephrotic, not nephritic).

❌ Lipiduria
Seen in nephrotic syndrome along with hyperlipidemia.

❌ Edema
Prominent in nephrotic syndrome; in nephritic syndrome, only mild edema may appear due to salt and water retention.

✅ Medullary collecting ducts
The nephron extends from Bowman’s capsule to the distal convoluted tubule. Collecting ducts are separate structures that drain multiple nephrons and are not technically part of the nephron itself.

The nephron is the structural and functional unit of the kidney. It consists of:

1. Renal corpuscle (glomerulus + Bowman’s capsule).

2. Proximal convoluted tubule.

3. Loop of Henle.

4. Distal convoluted tubule.

The collecting ducts are distinct — they receive urine from several nephrons and participate in final concentration under hormonal control (ADH, aldosterone). Thus, they are not strictly part of the nephron.

Explanation of the Incorrect Options

❌ Bowman’s capsule
Part of the renal corpuscle, essential to the nephron.

❌ Mesangial cells
Located within the glomerulus; provide structural support, phagocytosis, and regulate filtration. Considered part of the nephron’s functional unit.

❌ Loop of Henle
A clear segment of the nephron involved in countercurrent multiplication.

❌ Glomerulus
The capillary tuft of the renal corpuscle — the very start of the nephron.

✅ Hypertension
In chronic renal failure, sodium and water retention, along with activation of the renin–angiotensin–aldosterone system (RAAS), leads to systemic hypertension.

Chronic renal failure (CRF) leads to progressive loss of nephron function and several systemic complications:

• Hypertension: due to sodium and water retention + RAAS activation.

• Metabolic acidosis: impaired H⁺ excretion and decreased bicarbonate reabsorption.

• Hyperkalemia: impaired potassium excretion.

• Hypocalcemia & hyperphosphatemia: impaired vitamin D activation and phosphate retention → renal osteodystrophy.

• Normocytic, normochromic anemia: reduced erythropoietin production.

Thus, hypertension is a hallmark complication of CRF.

Explanation of the Incorrect Options

❌ Metabolic alkalosis
CRF leads to metabolic acidosis, not alkalosis.

❌ Hypernatremia
Sodium is usually retained with water, leading to isotonic or hyponatremic states, not hypernatremia.

❌ Hypokalemia
CRF causes hyperkalemia due to reduced excretion.

❌ Polyuria
Seen in early renal damage or diabetes insipidus; in advanced CRF, urine output often falls (oliguria).

✅ Diabetes insipidus
Loss of free water without proportional sodium loss leads to increased plasma sodium concentration (hypernatremia).

Hypernatremia occurs when there is a relative deficit of water compared to sodium.

• In diabetes insipidus (DI), whether central (↓ ADH) or nephrogenic (renal insensitivity to ADH), the kidneys fail to concentrate urine.

• This leads to excessive water loss (polyuria) while sodium is retained → plasma sodium rises.

• Clinically, patients present with polyuria, polydipsia, dehydration, and hypernatremia.

Explanation of the Incorrect Options

❌ Renal failure
Usually leads to hyponatremia or isotonic retention, because sodium and water handling are both impaired.

❌ Vomiting
Causes loss of gastric contents (rich in H⁺, Cl⁻, K⁺), often leading to hyponatremia due to volume depletion and secondary ADH release.

❌ Diarrhea
Typically causes hyponatremia or isotonic dehydration because sodium is lost along with water in stool.

❌ Coma
Not a primary cause of hypernatremia; however, impaired access to water in unconscious patients may worsen it secondarily.

✅ Glomerular basement membrane
The glomerular basement membrane (GBM) is the primary selective filtration barrier, allowing water and small solutes to pass while restricting plasma proteins and cells.

The glomerular filtration barrier is composed of three layers:

1. Fenestrated endothelium of glomerular capillaries – prevents blood cells from crossing.

2. Glomerular basement membrane (GBM) – thick, negatively charged structure that repels large and negatively charged proteins like albumin.

3. Podocyte slit diaphragms – provide the final size-selective barrier.

The GBM is particularly important as it provides both size selectivity and charge selectivity, ensuring that essential plasma proteins remain in circulation while waste and small solutes are filtered.

Explanation of the Incorrect Options

❌ Proximal convoluted tubule
Mainly involved in reabsorption of filtered solutes (glucose, amino acids, bicarbonate, sodium, water), not selective barrier function.

❌ Distal convoluted tubule
Involved in fine-tuning of electrolyte balance (Na⁺, K⁺, Ca²⁺), under hormonal control, not the primary selective barrier.

❌ Renal pelvis
A collecting space for urine; no role in selective filtration.

❌ Vasa recta
Capillaries that maintain medullary concentration gradient via countercurrent exchange; not a barrier to filtration.

✅ Urea
Urea is not a reliable marker of GFR because it is reabsorbed in the renal tubules, so its clearance underestimates true GFR.

Measurement of GFR:
An ideal marker for GFR should be:

• Freely filtered at the glomerulus.

• Not secreted, reabsorbed, metabolized, or synthesized by the kidneys.

Substances used:

• Inulin: Gold standard for GFR measurement.

• Iothalamate: A radiolabeled marker, commonly used clinically.

• Creatinine: Endogenous, approximate measure (slightly overestimates GFR because of tubular secretion).

• Cystatin C: A newer serum marker, useful especially when creatinine is unreliable.

Urea clearance is affected by tubular reabsorption (in dehydration) and is therefore unreliable as a direct measure of GFR, though it is used as part of BUN (blood urea nitrogen) in renal function assessment.

Explanation of the Incorrect Options

❌ Iothalamate
Used as an exogenous marker of GFR in clinical practice.

❌ Cystatin C
A low–molecular weight protein produced by all nucleated cells; its serum concentration reflects GFR accurately.

❌ Creatinine
An endogenous marker; widely used clinically though it slightly overestimates GFR.

❌ Inulin
The gold standard for GFR measurement — freely filtered, not secreted or reabsorbed.

❌ Urea
Not ideal due to reabsorption — clearance does not reflect true GFR.

✅ Glomerular capillary colloid osmotic pressure
The plasma proteins in glomerular capillaries exert an osmotic force that pulls water back into capillaries, strongly opposing filtration.

Glomerular filtration depends on the balance of Starling forces across the glomerular capillary wall:

• Forces favoring filtration:

  • Glomerular capillary hydrostatic pressure (≈ 60 mmHg) → major driving force for filtration.

• Forces opposing filtration:

  • Bowman’s capsule hydrostatic pressure (≈ 18 mmHg) → resists movement of fluid out of capillaries.

  • Glomerular capillary colloid osmotic pressure (≈ 32 mmHg) → generated by plasma proteins, strongly pulling fluid back.

Among the opposing forces, glomerular capillary colloid osmotic pressure is the most significant.

Explanation of the Incorrect Options

❌ Peritubular capillary hydrostatic pressure
This occurs after filtration, influencing tubular reabsorption, not glomerular filtration directly.

❌ Bowman’s capsule colloid osmotic pressure
Normally negligible, since proteins do not enter Bowman’s space under healthy conditions.

❌ Glomerular capillary hydrostatic pressure
This is the main driving force for filtration, not an opposing factor.

❌ Bowman’s capsule hydrostatic pressure
This does oppose filtration, but it is weaker (~18 mmHg) compared to the colloid osmotic pressure (~32 mmHg).

✅ Adenosine deaminase
One classical form of SCID is due to adenosine deaminase (ADA) deficiency, which leads to toxic metabolite accumulation and failure of T-, B-, and NK-cell development.

Severe combined immunodeficiency (SCID) is a group of genetic disorders causing profound defects in both humoral and cell-mediated immunity.

• ADA deficiency → accumulation of deoxyadenosine and dATP, which are toxic to lymphocytes → failure of development of T cells, B cells, and NK cells.

• Other causes include IL-2 receptor gamma chain mutation, JAK3 mutations, and RAG1/2 recombinase mutations, but ADA deficiency is the classic exam answer.

Explanation of the Incorrect Options

❌ Bruton tyrosine kinase
Defective in X-linked agammaglobulinemia (Bruton’s disease) — affects B cells only, not T cells or NK cells.

❌ Lymphocyte receptor
Not a specific entity; TCR/BCR recombination failure (RAG mutations) can cause SCID, but the best-defined deficiency here is ADA.

❌ None of these
Incorrect because ADA deficiency is a well-established cause of SCID.

❌ WASP gene
Mutated in Wiskott–Aldrich syndrome (triad: eczema, thrombocytopenia, immunodeficiency), not SCID.

✅ 14 L
Extracellular fluid (ECF) makes up about one-third of total body water, so 1/3 of 42 L ≈ 14 L.

Body fluid compartments:

• Total Body Water (TBW): ≈ 60% of body weight (42 L in a 70 kg person).

• Intracellular Fluid (ICF): ≈ 2/3 of TBW → about 28 L.

• Extracellular Fluid (ECF): ≈ 1/3 of TBW → about 14 L.

The ECF is further divided into:

• Plasma: ≈ 3.5 L (1/4 of ECF).

• Interstitial fluid: ≈ 10.5 L (3/4 of ECF).

This distribution is critical for understanding fluid shifts in clinical practice (e.g., IV fluids, dehydration, edema).

Explanation of the Incorrect Options

❌ 20 L
Too high — would be closer to half of TBW, not the normal 1/3.

❌ 23 L
This value is close to ICF, not ECF.

❌ 10 L
Lower than the actual — would underestimate ECF.

❌ 25 L
Also represents a volume closer to ICF, not ECF.

✅ 20%
The filtration fraction (FF) is normally about 20%, meaning one-fifth of renal plasma flow is filtered into Bowman’s capsule.

Filtration Fraction (FF) is defined as:

FF=GFRRPFFF = \frac{GFR}{RPF}FF=RPFGFR​

• Normal GFR ≈ 125 mL/min

• Normal RPF ≈ 600 mL/min

• Thus, FF ≈ 125 / 600 ≈ 0.2 (20%)

This means that about 20% of plasma entering the glomeruli gets filtered, while the rest continues into efferent arterioles and peritubular capillaries.

Explanation of the Incorrect Options

❌ 100%
Impossible — not all plasma entering the glomerulus is filtered; that would stop downstream blood flow.

❌ 33%
Too high — filtration is lower than one-third of renal plasma flow.

❌ 45%
Also too high — would represent pathological states, not normal physiology.

❌ 60%
Much too high; would imply dangerous over-filtration.

✅ NK cells, B cells, and T cells
SCID involves profound defects in both humoral (B-cell) and cell-mediated (T-cell) immunity, and in many forms, NK cells are also affected.

Severe combined immunodeficiency (SCID) is a group of genetic disorders characterized by a failure of lymphocyte development. Depending on the genetic mutation (e.g., IL-2 receptor gamma chain defect, adenosine deaminase deficiency, JAK3 mutation), there can be absent or non-functional T cells, B cells, and NK cells.

• T-cell defects → impaired cell-mediated immunity.

• B-cell defects → impaired antibody production (secondary to lack of T-cell help).

• NK-cell defects → due to cytokine signaling pathway mutations (e.g., IL-15 pathway).

Because multiple immune lineages are affected, patients present early with severe recurrent infections, failure to thrive, and require bone marrow transplantation for survival.

Explanation of the Incorrect Options

❌ NK cells and B cells
SCID typically involves T-cell deficiency as a central feature, so excluding T cells is incorrect.

❌ T cells and B cells
Partially correct but incomplete — many SCID variants also include NK-cell loss.

❌ NK cells only
Too limited — SCID is defined by combined deficiencies.

❌ T cells only
Would describe conditions like isolated T-cell immunodeficiency, not SCID.

✅ Dihydropteroate synthase
Sulfonamides are structural analogs of para-aminobenzoic acid (PABA) and competitively inhibit dihydropteroate synthase, blocking folate synthesis in bacteria.

Mechanism:

• Bacteria must synthesize their own folic acid de novo, unlike humans who obtain it from diet.

• Sulfonamides mimic PABA, a substrate for dihydropteroate synthase.

• By competitively inhibiting this enzyme, sulfonamides prevent formation of dihydropteroic acid, an essential precursor of folic acid.

• This blocks production of tetrahydrofolate (THF), required for nucleotide synthesis, thereby inhibiting bacterial growth (bacteriostatic effect).

Explanation of the Incorrect Options

❌ Dihydrofolate reductase
Inhibited by trimethoprim (prokaryotes) and methotrexate (eukaryotes), not by sulfonamides.

❌ Peptidyl transferase
Inhibited by chloramphenicol, which blocks peptide bond formation at the 50S ribosome.

❌ Amidotransferase
Important in purine synthesis but not the target of sulfonamides.

❌ Topoisomerase
Inhibited by fluoroquinolones (e.g., ciprofloxacin), not sulfonamides.

✅ Entire urethra in females
The pelvic part of the urogenital sinus develops into the prostatic and membranous urethra in males, and the entire urethra in females.

The urogenital sinus is divided into three parts during development:

1. Vesical part → forms most of the urinary bladder (except trigone, which is mesodermal from mesonephric ducts).

2. Pelvic part → gives rise to:

   • Entire urethra in females.

   • Prostatic urethra and membranous urethra in males.

3. Phallic part → contributes to development of the penile urethra in males and the vestibule of the vagina in females.

Thus, the pelvic part specifically accounts for the female urethra in its entirety.

Explanation of the Incorrect Options

❌ Base of the bladder
Formed from the vesical part of the urogenital sinus, not the pelvic part.

❌ Clitoral primordium
Arises from the genital tubercle, not from the urogenital sinus.

❌ Genital tubercle
A separate structure that gives rise to the clitoris in females and glans penis in males.

❌ Trigone
Derived from the incorporated caudal ends of the mesonephric ducts (mesodermal origin), not from the urogenital sinus.

✅ Kidney
The parallelogram of Morris is a surface anatomical landmark used to outline the position of the kidney on the posterior abdominal wall.

The parallelogram of Morris is a four-sided area drawn on the back to project the position of the kidney.

• The upper boundary is the 11th rib.

• The lower boundary is the iliac crest.

• The lateral boundary is the vertical line from the midpoint of the iliac crest (midaxillary line).

• The medial boundary is the line 2.5 cm from the midline.

Within this parallelogram lies the surface marking of the kidney, useful in clinical examination, surgery, and radiology for locating the renal angle and understanding relations.

Explanation of the Incorrect Options

❌ Bladder
Surface anatomy of the bladder is determined in the suprapubic region, not by Morris’ parallelogram.

❌ Stomach
The stomach’s surface anatomy is related to the left hypochondrium and epigastrium; it is not outlined using the parallelogram of Morris.

❌ Spleen
The spleen lies under the left 9th–11th ribs, along the long axis of the 10th rib — no parallelogram method is used.

❌ Liver
Liver surface anatomy uses percussion lines (midclavicular, midsternal), not Morris’ parallelogram.

✅ 300 mOsm/l
The filtrate formed in Bowman’s capsule is iso-osmotic to plasma, around 300 mOsm/L.

When blood plasma is filtered at the glomerulus into Bowman’s space, the process is essentially a sieving of water and small solutes without altering their relative concentrations. Large proteins and cells are excluded, but the proportion of electrolytes and small molecules remains the same as plasma.

Therefore, the initial glomerular filtrate has an osmolarity of ~300 mOsm/L, equal to plasma osmolarity. Changes in osmolarity occur later in the nephron depending on water and solute handling (e.g., becoming hypo-osmotic in the distal tubule or hyperosmotic in the medulla under ADH influence).

Explanation of the Incorrect Options

❌ 600 mOsm/l
This occurs in the medullary interstitium during countercurrent concentration, not in the initial filtrate.

❌ 125 mOsm/l
Not correct — though 125 ml/min is the normal GFR, it is not the osmolarity.

❌ 250 mOsm/l
This would be slightly hypo-osmotic but does not represent initial glomerular filtrate.

❌ 30 mOsm/l
Such low osmolarity occurs only in dilute urine, not in Bowman’s space.

✅ Increases glomerular filtration rate (GFR)
ANP dilates afferent arterioles and constricts efferent arterioles, raising GFR and leading to increased sodium and water excretion (natriuresis & diuresis).

ANP is secreted from the atria in response to atrial stretch due to increased blood volume. It acts as a counter-regulatory hormone to the renin–angiotensin–aldosterone system (RAAS).

• ANP dilates afferent arterioles and constricts efferent arterioles, both of which increase GFR.

• The increased GFR leads to more sodium and water being filtered.

• Additionally, ANP inhibits Na⁺ reabsorption in the collecting ducts and suppresses renin and aldosterone secretion.
  Overall, ANP promotes natriuresis (sodium loss) and diuresis (water loss), lowering blood volume and pressure.

Explanation of the Incorrect Options

❌ Causes vasodilation of the afferent arterioles
This is true, but not the main mechanism stated in the answer choice — dilation alone is part of the action, but the exam expects the overall effect of increasing GFR.

❌ Decreases glomerular filtration rate (GFR)
Opposite effect — ANP increases GFR, not decreases it.

❌ Decreases Na⁺ channels in principal cells
This is the effect of aldosterone antagonism (e.g., spironolactone, amiloride), not ANP’s direct action.

❌ Constricts efferent arterioles
ANP does cause some efferent constriction, but again, the main integrated effect is captured by increasing GFR.

✅ Rostral pontine tegmentum
The pontine micturition center (PMC, Barrington’s nucleus) in the rostral pontine tegmentum coordinates detrusor contraction with sphincter relaxation.

The pontine micturition center (PMC), located in the rostral pontine tegmentum, is the higher control center that organizes the act of urination. While the basic reflex arc for micturition lies in the sacral spinal cord (S2–S4), it is the PMC that integrates sensory signals from bladder stretch receptors and ensures coordinated activity.

• It activates parasympathetic efferents, causing detrusor muscle contraction.

• It simultaneously inhibits sympathetic and somatic outflow, leading to relaxation of the internal and external urethral sphincters.

• This coordination allows for voluntary and socially appropriate urination under cortical influence.

Thus, although the spinal cord mediates the primitive reflex, the rostral pontine tegmentum is the key reflex center that makes micturition controlled and efficient.

Explanation of the Incorrect Options

❌ Medulla oblongata
Controls autonomic centers like cardiovascular and respiratory rhythms, but not the micturition reflex.

❌ Hypothalamus
Influences autonomic and endocrine functions and can modulate bladder function, but is not the reflex center.

❌ Spinal cord
Contains the sacral reflex arc for bladder emptying, but without PMC input, voiding is uncoordinated and reflexive (seen in spinal cord injury).

❌ Cerebellum
Coordinates movement and balance but has no direct role in bladder reflexes.

✅ Hyperprolactinemia
It is not a characteristic feature of chronic renal failure; the main metabolic disturbances involve electrolytes, minerals, and blood pressure regulation.

In chronic renal failure (CRF), the kidneys progressively lose their ability to excrete electrolytes, regulate minerals, and maintain blood pressure. The typical biochemical abnormalities include:

• Hyperphosphatemia due to phosphate retention.

• Hypocalcemia because of impaired vitamin D activation and phosphate retention leading to secondary hyperparathyroidism.

• Hyperkalemia from reduced renal potassium excretion.

• Hypertension due to sodium and water retention and activation of the renin–angiotensin system.

While endocrine disturbances can occur in CRF (such as reduced erythropoietin → anemia, altered vitamin D metabolism, and sometimes changes in hormone clearance), hyperprolactinemia is not a hallmark feature. It may occasionally appear in advanced uremia due to reduced clearance, but it is not classically included in the “core abnormalities” of CRF.

Explanation of the Incorrect Options

❌ Hyperphosphatemia
Correctly seen in CRF because the kidney fails to excrete phosphate.

❌ Hypocalcemia
Occurs due to decreased calcitriol (active vitamin D) production and phosphate retention, leading to bone disease (renal osteodystrophy).

❌ Hyperkalemia
Seen due to impaired renal excretion of potassium, which can become life-threatening.

❌ Hypertension
Common in CRF due to fluid retention and RAAS activation.

❌ Hyperprolactinemia
Not a defining or consistent feature of CRF.

✅ Active transport
Sodium exits the cell across the basolateral membrane via the Na⁺/K⁺ ATPase pump, an active transport mechanism.

In the late distal convoluted tubule (DCT) and collecting duct, sodium is reabsorbed across the apical membrane mainly through epithelial sodium channels (ENaCs). Once inside the cell, sodium must cross the basolateral membrane to return to the blood. This occurs through the Na⁺/K⁺ ATPase pump, which actively transports sodium out of the cell into the interstitial fluid (and eventually the peritubular capillaries), while pumping potassium into the cell. This active transport maintains the low intracellular sodium concentration, which is essential for sodium reabsorption throughout the nephron.

Explanation of the Incorrect Options

❌ Sodium-hydrogen antiport
This operates mainly in the proximal tubule, exchanging luminal Na⁺ for H⁺ secretion — not in the late DCT basolateral membrane.

❌ Sodium-hydrogen ATPase
Such a pump does not exist in the nephron’s basolateral membrane; Na⁺ transport there is by Na⁺/K⁺ ATPase.

❌ Cotransport
Na⁺ cotransport (e.g., with glucose or amino acids) occurs in the proximal tubule, not in the late DCT basolateral side.

❌ Symport
Similar to cotransport, symport mechanisms are relevant in the early nephron, not at the basolateral exit of Na⁺ in the late DCT.

✅ The right renal vein is longer than the left
In fact, the left renal vein is longer than the right, as it must cross in front of the aorta to reach the IVC.

The arrangement of structures at the kidney hilum is clinically important. From anterior to posterior, the order is: renal vein → renal artery → renal pelvis (ureter origin). The renal artery divides into several segmental branches, the renal vein drains directly into the IVC, and while some variation can occur in accessory vessels, the general pattern holds true.

The left renal vein is distinctly longer than the right because it crosses the midline, passing anterior to the aorta and posterior to the superior mesenteric artery before draining into the IVC. The right renal vein, in contrast, drains directly into the IVC and is shorter.

Explanation of the Incorrect Options

❌ The renal artery divides into 3–5 segmental arteries at the hilum
This is true — these segmental arteries are end arteries, supplying distinct renal segments without significant collateral circulation.

❌ The renal pelvis is normally the most posterior of the three
Correct — the pelvis lies behind the artery and vein, forming the beginning of the ureter.

❌ The renal veins empty directly into the inferior vena cava
Correct — both renal veins ultimately drain straight into the IVC.

❌ The anatomy of the contents of the hilum can be variable
Correct — accessory renal arteries or variable arrangements of the hilum are well documented.

❌ The right renal vein is longer than the left
This is false — the left renal vein is the longer one.

✅ Dehydration
Because decreased renal perfusion leads to reduced GFR and accumulation of nitrogenous waste.

Prerenal azotemia is caused by conditions that reduce blood flow to the kidneys without intrinsic kidney damage. Dehydration, hemorrhage, or shock reduce effective circulating volume, leading to hypoperfusion. The kidneys initially remain structurally normal, but reduced perfusion decreases GFR, causing retention of BUN and creatinine. Importantly, the BUN:Creatinine ratio rises (>20:1) because urea reabsorption increases in the proximal tubule while creatinine is not reabsorbed.

Explanation of the Incorrect Options

❌ Benign prostatic hyperplasia
This causes postrenal azotemia by obstructing urinary outflow at the bladder neck, not prerenal hypoperfusion.

❌ Renal papillary necrosis
This is an intrarenal cause of azotemia, often due to diabetes mellitus, analgesic abuse, or sickle cell disease.

❌ Ureteral stones
Stones obstruct urinary outflow, causing postrenal azotemia, not prerenal.

❌ Rhabdomyolysis
Muscle breakdown releases myoglobin, which damages renal tubules, leading to intrarenal azotemia (acute tubular necrosis).

✅ Hypotension
Correct — the most common complication during hemodialysis. It results from rapid fluid removal (ultrafiltration), impaired autonomic response, or cardiac dysfunction. Symptoms include dizziness, nausea, cramps, and even syncope.

Hemodialysis is a life-saving therapy but is frequently associated with acute complications. Among them, intradialytic hypotension is the most common, as the cardiovascular system struggles to adapt to sudden volume shifts. Preventive strategies include slower fluid removal, adjusting dialysate sodium, and midodrine administration.

Explanation of the Incorrect Options

❌ Amyloidosis
Occurs in long-term dialysis patients due to deposition of β2-microglobulin in joints and bones, but it is not the most common abnormality overall.

❌ Depression
Common in patients with chronic kidney disease due to psychosocial stress, but not considered the most frequent acute complication of the dialysis procedure itself.

❌ Infection
A serious risk, especially with vascular access (catheters, fistulas), but less frequent than hypotension during sessions.

❌ Itching (pruritus)
A bothersome symptom in chronic renal failure due to uremia or phosphate retention, but again not the leading dialysis-related abnormality.

✅ Monosodium urate monohydrate crystals
Correct — these needle-shaped crystals deposit in joints and soft tissues in gout. They are negatively birefringent under polarized light, appearing yellow when parallel to the axis and blue when perpendicular.

Gout results from hyperuricemia, leading to precipitation of monosodium urate monohydrate crystals in joints, especially the first metatarsophalangeal joint (podagra). These crystals trigger intense inflammation via activation of the NLRP3 inflammasome, causing release of IL-1β and recruitment of neutrophils. Clinically, this presents as sudden, excruciating joint pain with swelling and erythema.

Explanation of the Incorrect Options

❌ Calcium pyrophosphate crystals
These are found in pseudogout (CPPD disease). They are rhomboid-shaped and show positive birefringence under polarized light (opposite of gout).

❌ Calcium carbonate crystals
Rarely seen in joints; not typical of gout.

❌ Sodium chloride crystals
Common table salt; not deposited in human joints under pathologic conditions.

❌ Hydroxyapatite crystals
Deposited in calcific tendinitis and some osteoarthritis cases, but not in gout.

Erythropoietin (EPO) is a glycoprotein hormone that regulates red blood cell (RBC) production.

• It is produced mainly by the peritubular interstitial fibroblast-like cells of the kidney, particularly in the renal cortex and outer medulla.

• EPO secretion is stimulated by hypoxia. Low oxygen tension is sensed by these cells, leading to stabilization of hypoxia-inducible factor (HIF), which promotes EPO gene transcription.

• The hormone then acts on the bone marrow to stimulate proliferation and differentiation of erythroid progenitors, increasing RBC count and oxygen-carrying capacity.

This is why patients with chronic kidney disease often develop anemia, due to insufficient EPO production.

Explanation of the Incorrect Options

❌ Gall bladder
Stores and concentrates bile; no role in hormone production like EPO.

❌ Bone marrow
This is the site where RBCs are produced, but the stimulus (EPO) comes from the kidney, not from the marrow itself.

❌ Spleen
Acts as a blood filter and site of old RBC destruction; it does not produce EPO.

❌ Thymus
Main site for T-cell maturation in childhood; unrelated to erythropoietin secretion.

✅ Kidney
Correct — the major site of EPO production in adults. (In the fetus, the liver also produces EPO significantly.)

The lymphatic drainage of the kidneys follows the renal veins and drains primarily into the para-aortic (lumbar) lymph nodes, which are located along the abdominal aorta near the origin of the renal arteries. This makes sense because the kidneys are retroperitoneal organs lying adjacent to the aorta. These nodes eventually drain into the cisterna chyli and then the thoracic duct.

Explanation of the Incorrect Options

❌ Pre-aortic nodes
These nodes lie in front of the aorta and are mainly responsible for drainage of the gastrointestinal tract (celiac, superior mesenteric, inferior mesenteric nodes), not the kidneys.

✅ Para-aortic nodes
Correct — the main lymphatic drainage site of the kidneys.

❌ Inguinal nodes
These drain the superficial perineum, lower limb, and abdominal wall below the umbilicus, but not deep retroperitoneal structures like the kidney.

❌ Thoracic nodes
There are mediastinal and thoracic lymph nodes, but the kidneys drain into abdominal para-aortic nodes before lymph flows into the thoracic duct.

❌ Celiac nodes
These are pre-aortic nodes that drain foregut structures (stomach, liver, pancreas, spleen, etc.), not the kidneys.

After blood passes through the glomerular capillaries, it exits via the efferent arteriole. From here:

• In cortical nephrons → the efferent arterioles drain into the peritubular capillaries, which surround the proximal and distal convoluted tubules. These vessels play a crucial role in reabsorption and secretion.

• In juxtamedullary nephrons → the efferent arterioles form the vasa recta, which descend into the medulla and maintain the countercurrent exchange system.

Thus, the general answer is peritubular capillaries, with vasa recta being a special subset for juxtamedullary nephrons.

Explanation of the Incorrect Options

❌ Inferior mesenteric vein
This drains blood from the large intestine, not from the kidney.

✅ Peritubular capillaries
Correct — main drainage of efferent arterioles (especially in cortical nephrons).

❌ Afferent arteriole
This brings blood into the glomerulus, not out of it.

❌ Capillary tuft
This is the glomerulus itself — where the efferent arteriole originates, not where it drains.

❌ Vasa recta
Partially correct for juxtamedullary nephrons, but the broader correct answer is peritubular capillaries, since they are universal for cortical nephrons.

The kidney is supported and held in position within the posterior abdominal wall mainly by:

• Perinephric (Gerota’s) fascia, which encloses the kidney and the perirenal fat.

• This fascia, along with surrounding fat (perinephric fat and paranephric fat), acts as a cushion and anchor, preventing excessive movement of the kidney.

• The renal vessels and pressure from surrounding abdominal structures also contribute, but the main supportive structure is the perinephric fascia.

Explanation of the Incorrect Options

❌ Median arcuate ligament
This is part of the diaphragm arching over the aorta; it does not support the kidney.

✅ Perinephric fascia
Correct — it surrounds and anchors the kidney with its fat capsule.

❌ Peritoneal fluid
This lubricates abdominal viscera within the peritoneal cavity. The kidneys are retroperitoneal and are not supported by peritoneal fluid.

❌ Greater omentum
A fold of peritoneum hanging from the stomach and transverse colon; it provides protection to abdominal viscera but has no role in supporting the kidneys.

❌ Lesser omentum
A peritoneal fold between the stomach/duodenum and liver; also unrelated to kidney support.

Hydronephrosis refers to dilation of the renal pelvis and calyces due to obstruction of urinary flow (e.g., from stones, strictures, tumors, or prostate enlargement). It is not a cystic disease of the kidney. Instead, it is a secondary change due to pressure buildup. There are no true cysts in hydronephrosis — just dilated collecting structures.

Explanation of the Incorrect Options

❌ Autosomal dominant tubulointerstitial kidney disease
A genetic disorder that causes small cortical cysts and progressive tubulointerstitial fibrosis, leading to chronic kidney disease. It is a true cystic disorder.

❌ Childhood polycystic kidney disease (Autosomal recessive PKD)
A congenital cystic disease caused by PKHD1 gene mutation, leading to bilaterally enlarged kidneys with radially arranged cysts. Often associated with congenital hepatic fibrosis.

❌ Adulthood polycystic kidney disease (Autosomal dominant PKD)
A common inherited cystic disorder due to mutations in PKD1 or PKD2 genes, characterized by large bilateral kidneys with multiple cysts. Often associated with intracranial aneurysms and liver cysts.

❌ Medullary sponge disease
A developmental anomaly where the collecting ducts in the medulla are cystically dilated, leading to nephrocalcinosis and recurrent urinary tract infections.

✅ Hydronephrosis
Not a cystic disease — it is due to obstruction causing back-pressure dilatation.

Orotic aciduria is the condition characterized by excessive orotate (orotic acid) in urine.
It results from a defect in the UMP synthase enzyme (part of pyrimidine synthesis pathway). This leads to accumulation of orotic acid, megaloblastic anemia (not responsive to B12 or folate), and growth retardation. Supplementation with uridine monophosphate (UMP) bypasses the enzyme defect and corrects the condition.

Explanation of the Incorrect Options

❌ Maple syrup urine disease
Caused by deficiency of branched-chain α-ketoacid dehydrogenase, leading to accumulation of leucine, isoleucine, and valine. Urine has a sweet, maple syrup-like odor — unrelated to orotate.

✅ Orotic aciduria
Correct. Characterized by orotic acid excretion due to pyrimidine metabolism defect.

❌ Phenylketonuria (PKU)
Due to deficiency of phenylalanine hydroxylase (or BH4 cofactor), leading to accumulation of phenylalanine and phenylketones in urine. Presents with intellectual disability, musty odor, and fair complexion.

❌ Homocystinuria
Results from cystathionine β-synthase deficiency or other homocysteine metabolism defects. Features include marfanoid habitus, lens subluxation, and predisposition to thrombosis.

❌ Alkaptonuria
Caused by homogentisate oxidase deficiency in tyrosine metabolism. Leads to homogentisic acid accumulation, causing dark urine, ochronosis (blue-black connective tissue pigmentation), and early-onset arthritis.

The proximal convoluted tubule (PCT) is lined by simple cuboidal epithelium. These cells are large, with a centrally placed nucleus and a dense brush border of microvilli on the apical surface. The brush border greatly increases surface area for reabsorption of water, electrolytes, glucose, and amino acids — which is why the PCT handles about 65–70% of the filtrate reabsorption. The presence of abundant mitochondria in these cells also supports their high metabolic activity.

Explanation of the Incorrect Options

❌ Pseudostratified columnar epithelium
This type is seen in parts of the respiratory tract (e.g., trachea, bronchi), not in renal tubules.

❌ Simple squamous epithelium
This lines structures specialized for passive diffusion (e.g., alveoli, Bowman’s capsule parietal layer, thin segments of the loop of Henle), not the PCT which requires active reabsorption.

❌ Simple columnar epithelium
This type is seen in absorptive linings like the gastrointestinal tract, not in the PCT.

❌ Transitional epithelium
Also called urothelium, this is found in the urinary bladder, ureters, and renal pelvis, not in the nephron tubules.

Antidiuretic hormone (ADH, also called vasopressin) is secreted by the posterior pituitary in response to increased plasma osmolality or decreased blood volume/pressure. Its primary action is on the collecting ducts of the nephron, where it binds to V₂ receptors. This stimulates insertion of aquaporin-2 channels into the apical membrane of collecting duct cells, allowing more water to be reabsorbed back into the bloodstream.
As a result, urine volume decreases (antidiuresis) and the urine becomes concentrated, while plasma osmolality decreases.

Explanation of the Incorrect Options

❌ Decreases sodium reabsorption
This is not the role of ADH. Sodium handling is mainly regulated by aldosterone, not ADH.

❌ Increases sodium reabsorption
Again, aldosterone — not ADH — is responsible for enhancing sodium reabsorption in the distal nephron.

✅ Increases water reabsorption
Correct. ADH specifically targets water permeability via aquaporins in collecting ducts.

❌ Decreases water reabsorption
This would be the effect of ADH deficiency (e.g., diabetes insipidus), but not the function of ADH itself.

❌ Increases urea secretion
ADH actually increases urea reabsorption in the inner medullary collecting ducts to help maintain the medullary osmotic gradient.

Net Filtration Pressure (NFP) in the kidney is the balance between forces that promote filtration and those that oppose it across the glomerular capillaries.

• Glomerular hydrostatic pressure (PG) ≈ 55 mmHg → pushes fluid out of capillaries.

• Blood colloid osmotic pressure (πG) ≈ 30 mmHg → pulls fluid back into capillaries.

• Capsular hydrostatic pressure (PC) ≈ 15 mmHg → resists filtration by pushing fluid back into the glomerulus.

So,
NFP = PG − (πG + PC) = 55 − (30 + 15) = 10 mmHg.

This positive pressure drives filtration of plasma into Bowman’s capsule. Even though the number seems small, it is physiologically sufficient to produce the normal GFR of ~125 ml/min.

Explanation of the Incorrect Options

❌ 20 mmHg
Too high; if NFP were this elevated, the GFR would be nearly doubled, which is not physiologic.

❌ 30 mmHg
This value corresponds more closely to the oncotic pressure, not to NFP itself.

❌ 25 mmHg
Not physiologic — this is higher than the actual driving pressure in healthy adults.

✅ 10 mmHg
Correct — the true net filtration pressure that sustains normal GFR.

❌ 15 mmHg
Closer than the higher values but still above the true average NFP.

The glomerular filtration rate (GFR) is the volume of filtrate formed per minute by both kidneys combined. In a healthy adult, the normal GFR is about 125 ml/min (which equals approximately 180 liters/day). This value represents the balance between hydrostatic and oncotic pressures across the glomerular capillaries. It is an essential measure of renal function and is often estimated clinically by clearance tests such as creatinine clearance.

Explanation of the Incorrect Options

❌ 100 ml/min
This is lower than normal and may indicate mild impairment of renal function, especially if persistent. It is below the standard physiologic reference value.

❌ 155 ml/min
This is higher than the normal physiologic range. Such a value might be seen transiently in hyperfiltration states (e.g., early diabetes mellitus, pregnancy) but is not the standard reference for healthy adults.

✅ 125 ml/min
Correct — the average normal GFR in a healthy adult.

❌ 150 ml/min
Like 155, this is above the normal resting range and not considered the baseline reference value.

❌ 175 ml/min
This is excessively high and not normal. If present, it may reflect pathological hyperfiltration and would likely damage glomeruli over time.

Nephrotic syndrome is a clinical condition characterized by massive proteinuria, hypoalbuminemia, edema, hyperlipidemia, and lipiduria.
The defining feature is proteinuria greater than 3.5 g per day in adults (or >40 mg/m²/hr in children). This high level of protein loss overwhelms the liver’s ability to synthesize albumin, leading to decreased plasma oncotic pressure and the development of edema.

Explanation of the Incorrect Options

>5.7 g/day
This value is not used in diagnostic criteria. Although proteinuria may sometimes exceed 5 g/day in severe cases, the diagnostic cutoff remains 3.5 g/day.

>9.4 g/day
This is excessively high and may occur in severe glomerular diseases (e.g., collapsing FSGS), but it is not the threshold used for diagnosis.

>30 g/day
Such a massive protein loss is not physiologically sustainable; it would rapidly deplete body proteins and is not part of the diagnostic definition.

>50 g/day
This is unrealistic and incompatible with life; the kidney cannot excrete such enormous amounts daily.

The nephron has portions that lie in both the renal cortex and the renal medulla. The proximal convoluted tubule (PCT) lies entirely within the renal cortex, near the glomerulus. This is where most reabsorption of water, electrolytes, glucose, and amino acids occurs. The PCT is a highly coiled segment and histologically lined with cuboidal epithelium with a dense brush border of microvilli, increasing surface area for reabsorption. Its location in the cortex is essential because it is closely associated with the glomerulus for immediate processing of filtrate.

Explanation of the Incorrect Options

Medullary collecting duct
As the name suggests, the medullary collecting ducts lie in the medulla, not in the cortex. They are involved in final concentration of urine under the influence of ADH.

Thin descending limb
This portion of the loop of Henle dips into the renal medulla. It is highly permeable to water, allowing water reabsorption into the hyperosmotic medullary interstitium.

Thin ascending limb
Like the thin descending limb, this segment is also located in the medulla. It is impermeable to water but allows passive transport of ions.

None of these
This would be incorrect because the proximal convoluted tubule clearly lies in the cortex.

During embryological development, the kidneys form in the pelvic region and normally ascend to their final position in the lumbar region. In the case of a horseshoe kidney, the lower poles of the two kidneys fuse, forming a U-shaped structure. When this fused kidney tries to ascend, it gets stopped by the inferior mesenteric artery (IMA), which arises from the aorta at the level of L3. Because the fused lower poles cannot pass beyond this vessel, the ascent halts, and the kidney remains lower than normal. This is a classic embryological point and explains why horseshoe kidneys are often found in the lower lumbar region.

Explanation of the Incorrect Options

Superior mesenteric artery (SMA)
Although the SMA is also a major branch of the abdominal aorta, it originates higher (around L1). By the time the horseshoe kidney ascends, it is already restricted by the IMA before it can reach the level of the SMA. Therefore, the SMA does not play a role in limiting ascent.

Abdominal aortic bifurcation
The aortic bifurcation into the common iliac arteries occurs at the level of L4. This point is below the origin of the IMA, so it cannot act as the barrier. In fact, if ascent were blocked here, the kidney would not even reach the lumbar region, which is not what we observe.

Urinary bladder
The bladder is located in the pelvis, and while it is related to the initial position of the developing kidneys, it does not interfere with their ascent. Once the kidneys begin migrating upward, the bladder stays behind in the pelvis, playing no role in restricting movement.

Ureter
The ureters elongate as the kidneys ascend, but they are flexible tubes that adapt to the kidney’s position. They do not mechanically restrict kidney ascent.