Chronic Kidney Disease

Chronic kidney disease (CKD) is characterized by a gradual, progressive loss of renal function and declining GFR (less than 60 ml/min/1.73 mt2 lasting for 3+ months). In the early stages, patients experience few signs or symptoms, and early detection can help prevent progression to renal failure. CKD was previously called "chronic kidney failure"; new terminology includes, but is not limited, to kidney failure. We can break the progression of CKD into 5 stages with decreasing renal functioning, increasing accumulation of toxins, and worsening uremia. End-stage renal disease (ESRD) is the terminal stage of kidney disease; GFR is less than 5% of normal. Renal failure is the result of excess retention of nitrogenous waste products and electrolyte disturbances that produce a variety of signs and symptoms. Read more about the 5 stages of chronic kidney disease.. Azotemia is increased blood urea nitrogen (BUN), creatinine, and other nitrogenous waste products in the blood (azot = nitrogen, emia = blood). Azotemia occurs in both acute kidney injury and chronic kidney disease. Uremia: Azotemia can lead to uremia, which is a clinical syndrome characterized by a cluster of signs/symptoms in various body systems, including the cardiac and nervous systems. Uremia can occur in acute kidney injury but is more common in chronic disease.

• Diabetes
• Hypertensive nephrosclerosis
• Glomerular disorders
• Autosomal dominant polycystic kidney disease

Be aware that episodes of Acute Kidney Injury put patients at higher risk of developing chronic kidney disease. Stages 1-4 are typically asymptomatic; thus, patients are often unaware that they have CKD until in ESRD. As GFR declines, symptoms appear gradually and are nonspecific. Signs and symptoms of uremia appear when nearing end-stage CKD, due to the metabolic disturbances caused by renal impairment:

• Anorexia, with nausea and vomiting
• Anemia and fatigue
• Pruritus (itching), edema, and uremic "frost" (deposition of urea crystals on the skin that are left behind when sweat evaporates)
• Muscle cramping and twitching
• Peripheral neuropathies, mental status changes, and seizures.

Uremia warrants hospitalization and dialysis. Persistent proteinuria with or without abnormal GFR for more than 3 months.

• Multiple assessments of GFR are tracked over time to determine rate of progression; watch for signs of injury that can be reversed.

Examples of Reversible Causes:

• Obstruction
• ECF fluid volume depletion/hypotension
• Hypercalcemia
• Nephrotoxic agents
• Severe/urgent hypertension
• Heart failure exacerbation

Bilateral echogenic kidneys on ultrasound is indicative of scarring Address underlying cause to slow progression of CKD. Patients should be counseled on personalized recommendations for dietary intake of protein, salt, water, potassium, and phosphorus to slow CKD progressions and mitigate complications. Patients' medication dosages may need to be adjusted for changes in GFR.

• For example, diabetic patients are at risk of hypoglycemia when renal elimination of insulin is decreased.
• Patients should avoid magnesium-containing medications (i.e. laxatives, antacids) and phosphorus-containing medicines (i.e., enemas).
• Avoid nephrotoxic drugs (including NSAIDS); limit PPI use.
• Beware of accumulated active morphine metabolites in advanced CKD.

Kidney replacement therapy is necessary for survival when GFR declines to 5-10 mL/min/1.73 m2.

• Hemodialysis, peritoneal dialysis, kidney transplantation.

Hypertension is a common complication of CKD due to impaired sodium excretion and resulting volume overload. Thus, hypertension can be both a cause and a consequence of CKD. Coronary artery disease Heart failure Atrial fibrillation Pericarditis Mineral bone disorders can occur when kidney disease interferes with vitamin D activation, leading to calcium/phosphate imbalances and bone pathologies (secondary hyperparathyroidism). Renal osteodystrophy is common in advanced CKD; osteitis fibrosa cystica is the most common. Osteitis fibrosa cystica is the result of secondary hyperparathyroidism with high bone resorption and subperiosteal lesions. Patients experience bone pain and proximal muscle weakness. Anemia is caused by decreased RBC formation due to impaired renal release of erythropoeitin (EPO). Coagulopathy can occur due to platelet dysfunction or severe anemia. More common in end stages of CKD. Review potassium balance. When the kidneys cannot perform their normal functions, nonanion gap metabolic acidosis develops.

• Because the bone buffers excess hydrogen ions, calcium and phosphorus is leached from the bone, resulting in bone disorders as described above.
• Chronic acidosis can lead to increased muscle protein catabolism and accelerate CKD progression.
• Chronic acidosis can inhibit growth in children.

Uremic encephalopathy is the result of accumulated uremic toxins. Early symptoms include difficulty concentration, which can progress to lethargy, confusion, seizure, and coma. Additional neurologic complications include peripheral neuropathies, autonomic dysfunction, restless leg syndrome, and erectile dysfunction. Hypothyroidism