genitourinary disorders
Chronic Kidney Disease
Pathophysiology of Chronic Kidney Disease
Chronic kidney disease (CKD) is initially described as diminished renal reserve or renal insufficiency, which may progress to renal failure (end-stage kidney disease). Initially, as renal tissue loses function, there are few noticeable abnormalities because the remaining tissue increases its performance (renal functional adaptation). Decreased renal function interferes with the kidneys’ ability to maintain fluid and electrolyte homeostasis. The ability to concentrate urine declines early and is followed by decreases in ability to excrete excess phosphate, acid, and potassium. When renal failure is advanced (glomerular filtration rate [GFR]≤15 mL/min/1.73 m2), the ability to effectively dilute or concentrate urine is lost; thus, urine osmolality is usually fixed at about 300 to 320 mOsm/kg, close to that of plasma (275 to 295 mOsm/kg), and urinary volume does not respond readily to variations in water intake. Plasma concentrations of creatinine andurea(which are highly dependent on glomerular filtration) begin a hyperbolic rise as GFR diminishes. These changes are minimal early on. When the GFR falls below 15 mL/min/1.73 m2(normal>90 mL/min/1.73 m2), creatinine andurealevels are high and are usually associated with systemic manifestations (uremia).Ureaand creatinine are not major contributors to the uremic symptoms; they are markers for many other substances (some not yet well-defined) that cause the symptoms. Despite a diminishing GFR, sodium and water balance is well-maintained by increased fractional excretion of sodium in urine and a normal response to thirst. Thus, the plasma sodium concentration is typically normal, and hypervolemia is infrequent unless dietary intake of sodium or water is very restricted or excessive. Heart Failure (HF) can occur due to sodium and water overload, particularly in patients with decreased cardiac reserve. For substances whose secretion is controlled mainly through distal nephron secretion (eg, potassium), renal adaptation usually maintains plasma levels at normal until renal failure is advanced or dietary potassium intake is excessive. Diuretics , (PTH), and Vitamin D Deficiency and Dependency can occur, as can renal osteodystrophy. Decreased renal production of Renal osteodystrophy(abnormal bone mineralization resulting from hyperparathyroidism,calcitrioldeficiency, elevated serum phosphate, or low or normal serum calcium) usually takes the form of increased bone turnover due to hyperparathyroid bone disease (osteitis fibrosa) but can also involve decreased bone turnover due to adynamic bone disease (with increased parathyroid suppression) or osteomalacia.Calcitrioldeficiency may cause osteopenia or osteomalacia. Moderate Metabolic Acidosis (plasma bicarbonate content 15 to 20 mmol/L) is characteristic. Acidosis causes muscle wasting due to protein catabolism, bone loss due to bone buffering of acid, and accelerated progression of kidney disease. stage 3). The anemia of CKD is normochromic-normocytic, with a hematocrit of 20 to 30% (35 to 40% in patients with Autosomal Dominant Polycystic Kidney Disease (ADPKD) ). It is usually caused by deficient 