Summary
Highlights
The kidney's functional unit is the nephron, and hormones like renin, aldosterone, and antidiuretic hormone (ADH) are crucial for water and electrolyte balance. Renin and aldosterone regulate sodium reabsorption and potassium secretion, impacting water movement. ADH moves water without sodium, concentrating urine. Kidneys also produce erythropoietin, renin, and activate vitamin D, influencing red blood cell production, blood pressure, and calcium metabolism.
Urine formation begins in the glomerulus, filtering blood plasma (excluding large proteins and fats). Most filtrate is reabsorbed in the tubules, with glucose having a threshold. Proteinuria can indicate glomerular damage, overflow of small proteins (like Bence Jones protein), or tubular damage. Tamm-Horsfall protein is secreted by kidneys, possibly preventing kidney stones.
Kidneys play a slower but vital role in acid-base balance by excreting excess acids or alkalis. They excrete hydrogen ions and reabsorb bicarbonate, crucial for buffering excess hydrogen ions and maintaining pH.
Uremic syndrome, characterized by azotemia (high BUN), is common in chronic kidney disease or acute injury. Kidney failure is defined by low GFR or creatinine clearance. Glomerulonephritis, inflammation of the glomerulus, often follows streptococcal infection and presents with proteinuria, edema, hematuria, and high blood pressure.
Nephrotic syndrome, linked to diabetes and lupus, involves heavy proteinuria, leading to hypoalbuminemia and edema. Renal tubular acidosis results from impaired bicarbonate reabsorption or hydrogen ion secretion. Urinary tract infections (UTIs) include cystitis (bladder inflammation) and pyelonephritis (kidney infection), with casts in urine indicating kidney involvement. Symptoms include fever and painful urination; for the elderly, altered mental state can be a sign.
Polycystic kidney disease is a genetic disorder causing cysts, leading to kidney transplant. Diabetic nephropathy is kidney damage from chronic high glucose, slowly decreasing renal function. Microalbumin testing detects early proteinuria to intervene and preserve kidney function.
Acute renal failure can be pre-renal (hypoperfusion), renal (kidney disease, toxins), or post-renal (obstruction). Resolving the cause often reverses acute failure. Chronic renal failure is a progressive loss of function, common in chronic diseases like diabetes or prolonged hypertension. Diabetes insipidus, distinct from diabetes mellitus, is a failure of water reabsorption due to ADH deficiency (neurogenic) or resistance (nephrogenic), causing excessive dilute urine production.
Renal obstruction, causing post-renal azotemia, can be due to kidney stones (renal calculi), enlarged prostates, tumors, or blood clots. Kidney stones are crystalline aggregates influenced by diet, dehydration, and genetics. Diagnosis involves imaging, urinalysis (for crystals), and BUN/creatinine levels.
Urinalysis involves physical, chemical, and microscopic examination to diagnose, screen, and monitor kidney disease. Blood urea nitrogen (BUN) measures a protein catabolism waste product; elevated BUN indicates decreased glomerular function. Creatinine, a muscle waste product, is consistently produced and freely filtered, making it a reliable indicator of renal function and damage severity.
The BUN/creatinine ratio distinguishes types of azotemia: normal ratio with high levels suggests renal azotemia, while a ratio >20:1 often indicates pre-renal azotemia. Creatinine clearance, calculated from 24-hour urine and serum samples, estimates GFR. Uric acid, a purine metabolism product, can cause kidney stones and is elevated in conditions like gout or increased cell turnover.
Urine protein indicates renal disease and can be measured by dipstick or automated chemistry. Urine osmolality measures urine concentration, aiding in diabetes insipidus diagnosis. End-stage renal disease is treated with hemodialysis (machine filters blood) or peritoneal dialysis (peritoneal cavity used for waste removal).