Certified Dialysis Nurse (CDN) Exam

The kidneys are paired, bean-shaped organs located retroperitoneally in the posterior abdominal cavity. Each kidney measures approximately 11–12 cm in length, 5–6 cm in width, and 3 cm in thickness. The adult kidney weighs approximately 150 grams. The right kidney sits slightly lower than the left due to displacement by the liver.

Each kidney contains approximately 1 million nephrons, which are the functional units responsible for urine formation. The nephron consists of the glomerulus, Bowman's capsule, proximal convoluted tubule, loop of Henle, distal convoluted tubule, and collecting duct.

The kidneys filter approximately 180 liters of plasma daily through the glomeruli, producing about 1–2 liters of urine. This filtration process removes metabolic waste products from the blood.

Urea is the primary nitrogenous waste product derived from protein metabolism. Normal blood urea nitrogen (BUN) ranges from 7–20 mg/dL. Elevated BUN indicates impaired renal excretion or increased protein catabolism.

Creatinine is a waste product of muscle metabolism. Normal serum creatinine ranges from 0.6–1.2 mg/dL in adults. Creatinine clearance serves as the gold standard for estimating glomerular filtration rate (GFR). Normal GFR is 90–120 mL/min/1.73 m².

Uric acid is produced from purine metabolism. The kidneys excrete approximately 70% of daily uric acid production. Impaired renal function leads to hyperuricemia and potential gout.

The kidneys maintain fluid balance by adjusting urine volume based on hydration status. Antidiuretic hormone (ADH) from the posterior pituitary regulates water reabsorption in the collecting ducts. When plasma osmolality rises, ADH secretion increases, promoting water retention and concentrated urine production.

Sodium regulation occurs primarily in the proximal tubule, where 65–70% of filtered sodium is reabsorbed. The renin-angiotensin-aldosterone system (RAAS) fine-tunes sodium balance. Aldosterone promotes sodium reabsorption in the distal tubule and collecting duct in exchange for potassium excretion.

Potassium homeostasis depends heavily on renal excretion. Approximately 90% of daily potassium intake is excreted by the kidneys. Normal serum potassium ranges from 3.5–5.0 mEq/L. Hyperkalemia is a life-threatening complication of renal failure.

Calcium and phosphorus balance involves complex interactions between the kidneys, bone, and parathyroid glands. The kidneys convert 25-hydroxyvitamin D to active 1,25-dihydroxyvitamin D (calcitriol), which promotes intestinal calcium absorption.

Magnesium regulation occurs primarily through renal excretion. Approximately 80% of plasma magnesium is filtered at the glomerulus, with most reabsorbed in the loop of Henle.

The kidneys maintain blood pH within the narrow range of 7.35–7.45 through three primary mechanisms.

Bicarbonate reabsorption occurs in the proximal tubule. Approximately 80–90% of filtered bicarbonate is reclaimed here through the action of carbonic anhydrase.

Hydrogen ion secretion takes place throughout the nephron. The distal tubule and collecting duct can secrete hydrogen ions against a concentration gradient, lowering urine pH to as low as 4.5.

Ammonium production and excretion serve as a buffer system. Glutamine metabolism in proximal tubule cells generates ammonia, which combines with hydrogen ions to form ammonium for excretion.

Renal compensation for respiratory acid-base disorders occurs over 3–5 days. In respiratory acidosis, the kidneys increase bicarbonate reabsorption. In respiratory alkalosis, bicarbonate excretion increases.

Erythropoietin (EPO) production occurs primarily in the peritubular interstitial cells of the renal cortex. EPO stimulates red blood cell production in the bone marrow. Hypoxia is the primary stimulus for EPO release. Renal failure results in decreased EPO production and normocytic, normochromic anemia.

Renin secretion occurs in the juxtaglomerular cells of the afferent arteriole. Renin converts angiotensinogen to angiotensin I, initiating the RAAS cascade. Stimuli for renin release include decreased renal perfusion pressure, decreased sodium delivery to the macula densa, and sympathetic nervous system activation.

Calcitriol synthesis is the final step in vitamin D activation. The enzyme 1-alpha-hydroxylase in the proximal tubule converts 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D. Calcitriol promotes intestinal calcium and phosphorus absorption and facilitates bone mineralization.

Prostaglandin production in the kidneys modulates renal blood flow and sodium excretion. Prostaglandins counteract the vasoconstrictive effects of angiotensin II and catecholamines.

The kidneys regulate blood pressure through multiple mechanisms. Volume regulation adjusts extracellular fluid volume by modifying sodium and water excretion. The RAAS system responds to decreased renal perfusion by promoting vasoconstriction and sodium retention. Natriuretic peptide receptors in the kidney respond to atrial natriuretic peptide (ANP), promoting sodium excretion and vasodilation. Prostaglandins and nitric oxide produced in the kidney contribute to vascular tone regulation.

The kidneys contribute to glucose homeostasis through gluconeogenesis, particularly during fasting states. The renal cortex can produce glucose from lactate, glutamine, and glycerol. During prolonged fasting, the kidneys may contribute up to 40% of total gluconeogenesis.