Renal 212

What is the functional filtering unit of the kidney?

The Nephron.

What normal range defines adult Serum Creatinine?

0.6 to 1.5 mg/dL.

Why is Serum Creatinine the single best lab indicator of GFR?

Produced at a constant muscle rate; freely filtered without tubular reabsorption.

What percentage reduction in GFR occurs when serum creatinine doubles?

Approximately 50% reduction in GFR.

What is the normal specific gravity range of human urine?

1.010 to 1.030.

What does a fixed urine specific gravity of 1.010 (isosthenuria) indicate?

Severe renal tubular damage resulting in total loss of concentrating/diluting ability.

What normal BUN range is expected in healthy adults?

8 to 25 mg/dL.

Why is Blood Urea Nitrogen (BUN) less specific for GFR than creatinine?

BUN varies with dietary protein intake, hydration, tissue breakdown, and GI bleeding.

What is the most common chemical composition of kidney stones (65–80%)?

Calcium Oxalate (or Calcium Phosphate).

What urine pH favors Calcium Oxalate kidney stone formation?

Alkaline urine pH.

What organism type drives Struvite (Staghorn) renal stone formation?

Urease-producing bacteria (e.g., Proteus mirabilis).

What chemical components comprise Struvite kidney stones?

Magnesium, Ammonium, and Phosphate.

What urine pH favors Uric Acid kidney stone formation?

Acidic urine pH (< 5.5).

What classic pain pattern identifies acute renal colic from a kidney stone?

Flank pain radiating down to the groin, testicles, or labia.

What structural condition defines Hydronephrosis?

Dilation of the renal pelvis and calyces due to urinary obstruction.

How does urinary obstruction cause permanent renal parenchymal injury?

Increased retrograde pressure compresses peritubular capillaries, causing ischemic renal atrophy.

What anatomical defense mechanism prevents bladder urine reflux into ureters?

Competence of the Ureterovesical Junction (UVJ).

What is the "washout phenomenon" in urinary tract defense?

Complete periodic bladder voiding physically flushes bacteria out of the urethra.

What anatomical site is inflamed in Uncomplicated Cystitis?

Bladder mucosa (Lower Urinary Tract).

What cardinal symptoms identify Cystitis?

Dysuria, urinary frequency, urgency, suprapubic pain, and pyuria (NO fever).

What anatomical site is inflamed in Acute Pyelonephritis?

Renal parenchyma and renal pelvis (Upper Urinary Tract).

What cardinal clinical signs differentiate Pyelonephritis from Cystitis?

Fever, chills, Costovertebral Angle (CVA) flank tenderness, and WBC casts in urine.

What microscopic urinalysis finding confirms Pyelonephritis?

White Blood Cell (WBC) casts.

What immune mechanism causes Acute Postinfectious Glomerulonephritis (PIGN)?

Type III immune complex deposition in glomeruli following Group A Beta-Hemolytic Strep.

What classic urine appearance identifies acute glomerulonephritis?

"Cola-colored" or smoky brown urine (hematuria with RBC casts).

What clinical tetrad characterizes nephritic syndrome in PIGN?

Hematuria, facial/periorbital edema, hypertension, and oliguria.

What defines Prerenal Acute Kidney Injury (AKI)?

Renal hypoperfusion without structural damage to nephron parenchyma.

What common clinical conditions trigger Prerenal AKI?

Hypovolemia, severe dehydration, hemorrhage, shock, and heart failure.

Is Prerenal AKI reversible?

Yes; rapidly reversible upon restoring renal blood flow and volume.

What defines Intrarenal AKI?

Structural parenchymal damage to glomeruli or renal tubules.

What is the most common cause of Intrarenal AKI in hospitalized patients?

Acute Tubular Necrosis (ATN) from ischemia or nephrotoxins.

What classic medication class acts as a primary nephrotoxin causing ATN?

Aminoglycoside antibiotics (e.g., Gentamicin).

What cellular events occur in tubular nephron cells during ATN?

Tubular cell necrosis, sloughing, cast formation, and tubular fluid backleak.

What defines Postrenal AKI?

Acute obstruction to urine outflow downstream from the kidneys.

What common structural condition causes Postrenal AKI in elderly men?

Benign Prostatic Hyperplasia (BPH).

What daily urine volume defines Oliguria in AKI?

Less than 400 mL/day in adults.

What daily urine volume defines Anuria in AKI?

Less than 50 mL/day (or total absence of urine).

What electrolyte imbalance poses the greatest cardiac hazard during the Oliguric Phase of AKI?

Severe Hyperkalemia (> 6 mEq/L).

What acid-base imbalance develops during the Oliguric Phase of AKI?

Metabolic Acidosis (due to impaired H+ secretion and loss of HCO3- regeneration).

What defines the Diuretic Phase of AKI?

Progressive rise in urine output (1 to 5 L/day) as renal function returns.

What mechanism drives high urine volume during the Diuretic Phase?

Osmotic diuresis caused by high blood urea and unhealed tubular concentrating ability.

What clinical risks threaten patients during the Diuretic Phase of AKI?

Severe dehydration, hypovolemia, hypotension, and hypokalemia.

What defines the Recovery Phase of AKI?

Normalization of GFR, serum creatinine, BUN, and electrolyte balance (takes 3–12 mos).

What clinical criterion defines Chronic Kidney Disease (CKD)?

GFR less than 60 mL/min for 3 consecutive months or longer.

What stage of CKD represents End-Stage Renal Disease (ESRD)?

Stage 5 CKD (GFR < 15 mL/min, requiring dialysis or transplant).

What sequence of events causes Renal Osteodystrophy in CKD?

Loss of Vit D activation -> Hypocalcemia -> Secondary Hyperparathyroidism -> PTH bone resorption.

Why does Hyperphosphatemia develop in Chronic Kidney Disease?

Failing kidneys cannot excrete phosphate, leading to high serum phosphate levels.

Why does Severe Anemia develop in Stage 4/5 CKD?

Parenchymal destruction leads to loss of Erythropoietin (EPO) synthesis by kidneys.

What respiratory pattern compensates for metabolic acidosis in uremia?

Kussmaul respirations (deep, rapid breathing blowing off CO2).

What causes Uremic Pruritus (severe skin itching) in ESRD?

Calcium-phosphate microcrystal deposition in skin tissue.

What skin appearance is produced by uremic pigment retention?

Yellow-sallow skin tone (retained urochromes).

What cardiovascular complication is the leading cause of death in CKD?

Hypertension and heart failure (due to volume overload and RAAS activation).

What is the physiological action of Erythropoietin (EPO)?

Stimulates red blood cell production in bone marrow.

Where is active Vitamin D (1,25-dihydroxycholecalciferol) synthesized?

Hydroxylated in proximal renal tubule cells of the kidney.

How does active Vitamin D affect intestinal calcium absorption?

Promotes active transport and absorption of dietary calcium in the gut.

What is Azotemia?

Accumulation of nitrogenous waste products (BUN and creatinine) in blood without overt symptoms.

What is Uremia?

Systemic toxic clinical syndrome resulting from severe renal failure (azotemia + symptoms).

What neurological signs characterize Uremic Encephalopathy?

Lethargy, confusion, peripheral neuropathy, asterixis, seizures, and coma.

What pericardial complication occurs in severe uremia?

Uremic Pericarditis (friction rub, chest pain).

What causes dilutional hyponatremia in AKI/CKD?

Impaired water excretion expanding intravascular fluid volume.

What hormone released by the adrenal cortex regulates renal sodium reabsorption?

Aldosterone.

What hormone released by the posterior pituitary regulates renal water reabsorption?

Antidiuretic Hormone (ADH / Vasopressin).

Where does ADH exert its physiological effect in the nephron?

Collecting Ducts (increasing aquaporin water channels).

What enzyme is released by juxtaglomerular cells in response to low renal blood pressure?

Renin.

What potent vasoconstrictor is generated by ACE action on Angiotensin I?

Angiotensin II.

What two systemic effects are produced by Angiotensin II?

Systemic arterial vasoconstriction and aldosterone release.

What normal GFR range defines Stage 1 CKD?

GFR >= 90 mL/min with demonstrated kidney damage.

What GFR range defines Stage 2 CKD?

GFR 60 to 89 mL/min (mild GFR reduction).

What GFR range defines Stage 3 CKD?

GFR 30 to 59 mL/min (moderate GFR reduction).

What GFR range defines Stage 4 CKD?

GFR 15 to 29 mL/min (severe GFR reduction).

What GFR range defines Stage 5 CKD (ESRD)?

GFR < 15 mL/min (renal failure).

What defines Proteinuria (Albuminuria) in renal glomerular disease?

Excretion of abnormal protein amounts (>300 mg/day) in urine due to podocyte damage.

What defines Nephrotic Syndrome?

Massive proteinuria (>3.5 g/day), hypoalbuminemia, severe generalized edema, and hyperlipidemia.

Why does Generalized Edema (Anasarca) occur in Nephrotic Syndrome?

Massive urinary loss of albumin lowers plasma oncotic pressure, driving fluid into tissue.

What defines Nephritic Syndrome?

Glomerular inflammation with hematuria (RBC casts), mild proteinuria, oliguria, and hypertension.

What renal structure is damaged to allow RBCs to leak into urine forming RBC casts?

Glomerular capillary basement membrane and podocytes.

What type of urinary cast indicates renal tubular epithelial cell death?

Granular or epithelial cell casts.

What type of urinary cast indicates end-stage chronic renal failure?

Broad, waxy casts.

Why does metabolic acidosis occur in chronic kidney failure?

Inability of damaged nephrons to secrete H+ ions and reabsorb/generate bicarbonate.

What electrolyte imbalance occurs alongside secondary hyperparathyroidism in CKD?

Hyperphosphatemia combined with Hypocalcemia.

What soft tissue complication results from elevated calcium-phosphate product in CKD?

Metastatic calcification in blood vessels, skin, heart, and joints.

What is uremic frost?

Evaporated urea crystal deposits on skin in extreme ESRD.

What GI symptoms result from uremic toxin buildup?

Uremic fetor (ammonia breath), metallic taste, anorexia, nausea, vomiting, and PUD.

Why is bleeding risk increased in uremia despite normal platelet counts?

Uremic toxins cause platelet dysfunction (impaired aggregation).

What glucose abnormality occurs in non-diabetic ESRD patients?

Insulin resistance due to uremic toxins.

How does severe hypovolemic shock cause Prerenal AKI?

Low arterial pressure drops renal perfusion below autoregulatory thresholds.

How does contrast dye (radiocontrast) cause Intrarenal AKI?

Induces renal vasoconstriction and direct tubular cell toxicity (radiocontrast nephropathy).

What mechanism causes Postrenal AKI from bilateral ureteral stone impaction?

Retrograde fluid pressure buildup back into nephrons, stopping filtration.

What urine osmolality characterises Prerenal AKI versus ATN?

Prerenal urine is concentrated (>500 mOsm/kg); ATN urine is isosthenuric (~300 mOsm/kg).

What Fractional Excretion of Sodium (FENa) characterises Prerenal AKI?

FENa < 1% (tubules reabsorb sodium to expand volume).

What Fractional Excretion of Sodium (FENa) characterises Intrarenal ATN?

FENa > 2% (damaged tubules lose sodium reabsorption ability).

What urine output threshold defines anuria?

Less than 50 mL/day.

What dietary restriction is required for potassium in oliguric AKI?

Strict potassium restriction to prevent lethal dysrhythmias.

Why is fluid intake restricted in oliguric renal failure?

Prevents pulmonary edema, hyponatremia, and severe hypertension (Formula: Previous 24h output + 500 mL).

What mechanism causes hypertension in chronic renal disease?

Sodium/water retention and hypersecretion of Renin (RAAS activation).

Why does polyuria occur in early Stage 3 CKD?

Solute diuresis in remaining functional nephrons and loss of concentrating ability.

What happens to drug clearance in renal failure?

Significantly decreased, requiring dose reduction to prevent toxicity.

What electrolyte abnormality causes neuromuscular irritability/tetany in CKD?

Hypocalcemia.

What arterial blood gas finding is expected in ESRD?

Metabolic Acidosis (low pH, low HCO3-).

What single blood test is used to stage Chronic Kidney Disease?

Estimated Glomerular Filtration Rate (eGFR).