Renal Metabolic Complications

Chronic kidney disease disrupts multiple metabolic processes, and the complications become more likely as glomerular filtration declines. Loss of functioning nephrons affects filtration, electrolyte and acid excretion, hormone production, and clearance of uraemic waste. Reduced erythropoietin production by the renal peritubular interstitial cells limits bone-marrow red-cell production. Uraemic conditions can also shorten red-cell survival, while inflammation and iron restriction reduce the response to erythropoietin. The resulting anaemia is usually normocytic and normochromic, although coexisting iron, vitamin B12, or folate deficiency can change the indices. Phosphate retention is an early driver of CKD-mineral and bone disorder. As phosphate rises, calcium balance and active vitamin D production are affected; parathyroid hormone then increases to maintain serum calcium. Persistent secondary hyperparathyroidism increases bone turnover and contributes to renal osteodystrophy, leaving bones more vulnerable to pain, deformity, and fracture. The kidneys normally excrete hydrogen ions and regenerate bicarbonate. With advanced CKD, impaired acid handling can produce metabolic acidosis, which promotes muscle protein catabolism and may worsen potassium elevation by shifting potassium out of cells. At the same time, reduced filtration limits urinary potassium excretion....