554 UNIT VIII RENAL AND UROLOGICAL DISORDERS
asymptomatic, and blood and urine tests may appear normal because the functioning nephrons compensate for the damaged nephrons. Hyperfiltration and hyper- trophy of the functioning nephrons maintain normal kidney function. In stage 3, there is diminished renal function, and symptoms start to become apparent because less than 50% of nephrons are functioning. In this stage, there is moderate reduction in GFR, serum creatinine and BUN begin to rise, and creatinine clearance starts to decrease. The functioning nephrons start to become unable to compensate for the lost nephrons. The dam- aged nephrons start to undergo fibrosis, and glomer- ulosclerosis is apparent on renal biopsy. In stage 4, a state of renal insufficiency becomes apparent. Neph- rons start to become overwhelmed, and GFR is lower than 20% of normal. The kidney’s health is precarious in this stage. The patient must restrict dietary protein because remaining healthy nephrons have difficulty removing nitrogenous wastes from the bloodstream. Finally, in stage 5, renal failure develops and GFR falls to less than 5% of normal. At this stage, nephrons can- not accomplish complete filtration of the bloodstream. The kidney’s varied functions, such as erythropoietin synthesis, blood pressure maintenance, and acid–base balance, are lost. As a consequence, fluid, electrolyte, and acid–base imbalances occur, and effects on other organ systems become apparent. ESRD occurs with widespread effects of uremia. The term “uremia” actu- ally means urine in the bloodstream. Uremia leads to disturbances in the function of virtually every organ system. The kidneys deteriorate in function and begin to atrophy. Dialysis and renal transplant are the only options for survival. Clinical Presentation In CKD, accumulation of nitrogenous wastes causes systemwide symptoms. The brain cannot function in a high nitrogenous environment and encepha- lopathy occurs—confusion, disorientation, or stupor and coma. Platelets and RBCs lyse because of the blood’s high nitrogen content, resulting in throm- bocytopenia and anemia. Thrombocytopenia causes bruising and spontaneous bleeding, whereas anemia causes severe fatigue, weakness, and dyspnea. Meta- bolic acidosis and electrolyte imbalances have vary- ing effects. Hyperkalemia can cause life-threatening cardiac dysrhythmias and extreme muscle weakness. Because the kidneys cannot synthesize vitamin D, calcium absorption from the gastrointestinal tract decreases, causing hypocalcemia, which in turn can cause neuromuscular irritability, tetany, and seizures. Hypocalcemia also stimulates the parathyroid glands to release parathyroid hormone (PTH), which causes bone breakdown. This bone demineralization process is referred to as renal osteodystrophy . Bone min- eral density is diminished, and fracture susceptibil- ity increases. Peripheral and autonomic neuropathy
BOX 22-2. Causes of Chronic Kidney Disease
There are many different etiologies and risk factors for CKD. Many different conditions can lead to CKD. The two most common are DM and HTN. • Family history of kidney disease • Age greater than 60 years • Atherosclerosis • Bladder obstruction
• Chronic glomerulonephritis • Congenital kidney disease • Diabetes • HTN • Systemic lupus erythematosus • Overexposure to some toxins • Sickle cell disease • Nephrotoxic medications
Pathophysiology The pathological changes that occur in CKD are due to significant deterioration of nephrons. CKD is defined as abnormal kidney structure or function lasting more than 3 months with associated health implications. Indicators of CKD include albuminuria, urine sedi- ment abnormalities, abnormal renal imaging findings, serum electrolyte or acid–base imbalances, and GFR less than 60 mL/minute per 1.73 m 2 . The patient’s GFR needs to be calculated using age, sex, and serum creatinine of the individual. To calculate GFR, cli- nicians commonly use the Chronic Kidney Disease Epidemiology Collaboration equation (http://www. kidney.org/professionals/kdoqi/gfr_calculator.cfm). CKD can have an insidious onset based upon etiology. The rate of nephron deterioration differs according to etiology and can range from several months to many years. According to the National Kidney Foundation, the progression of CKD usually occurs in five stages: • Stage 1: kidney damage with normal GFR (greater than 90 mL/min) • Stage 2: mild reduction in GFR (60 to 89 mL/min) • Stage 3: moderate reduction in GFR (30 to 59 mL/ min) • Stage 4: severe reduction in GFR (15 to 29 mL/min) • Stage 5: kidney failure (GFR lower than 15 mL/min) Glomerular filtration of the bloodstream is accom- plished by approximately 1 million nephrons in each kidney. The kidney is a resilient organ because of its huge number of nephrons, more than double the number necessary for maintenance of normal GFR (90 to 120 mL/min). Thus, normal filtration of the blood is possible with only one kidney. With mild kid- ney damage, which occurs in stages 1 and 2, filtration problems usually do not occur. The patient is usually
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