CHAPTER 22 Renal Disorders 553
are used in the diagnosis of AKI. Buildup of nitrogenous wastes in the blood, manifested as an elevated BUN, is a hallmark of AKI. When BUN rises >100 mg/dL, mental status changes and thrombocytopenia can occur. Analysis of the urinary sediment by a nephrolo- gist can lead to confirmation of the cause of AKI. For example, prerenal azotemia usually presents with unremarkable urinary sediment. Proteinuria suggests damage to the glomerulus. AKI due to ATN usually yields pigmented “muddy brown” casts. Glomerulonephritis can yield red blood cells or red blood cell casts in the urine. The CBC will commonly reveal anemia. AKI often leads to hyperkalemia, hyperphosphatemia, hypocal- cemia, and metabolic acidosis. Other recommended laboratory blood tests that can indicate glomerulone- phritis and vasculitis include low complement levels, antinuclear antibodies, antineutrophil cytoplasmic antibodies (ANCAs), and anti-GBM antibodies. There are biomarkers for AKI including kidney injury molecule (KIM-1), which can be detected in the urine and blood after ischemic or nephrotoxic injury. Neutrophil gelatinase associated lipocalin (NGAL) is present in blood and urine in inflammatory conditions of the kidney. Radiographic imaging may be used to assess for any type of obstructive process or changes in the kidneys’ size and structure. Findings of obstruction include dilation of the kidney pelvis and hydronephrosis. Vascular imaging may be useful if venous or arterial obstruction is suspected, but the risks of contrast dye administration should be kept in mind. MRI with gadolinium-based contrast agents should be avoided. A renal biopsy may be used to evaluate for intrarenal etiology of AKI. Treatment In 2012, Kidney Disease: Improving Global Outcomes (KDIGO) published a guideline on the classification and management of AKI. Since then, some new evi- dence has arisen that has implications for clinical practice. In general, management principles for AKI include determination of volume status, fluid resus- citation with isotonic crystalloid, treatment of volume overload with diuretics, discontinuation of nephro- toxic medications, and adjustment of prescribed drugs according to renal function. Additional supportive care measures include optimizing nutritional status and glycemic control. Treatment of AKI depends on the underlying cause. With prerenal AKI, fluid administration is indicated. Crystalloid solutions such as lactated Ringer’s solu- tion are recommended. Once the patient develops oli- guria, diuretics such as furosemide (Lasix) may be used cautiously. Electrolytes are monitored; with hyperka- lemia, cardiac monitoring is necessary. Discontinua- tion of renin-angiotensin-aldosterone inhibitors and NSAIDs is recommended. Pharmacist consultation on the effect of patient medications on renal function is
recommended. In patients who do not have rapid res- olution of AKI, continuous renal replacement therapy (CRRT) or hemodialysis may be indicated. Patients with AKI requiring renal dialysis and other forms of renal replacement therapy are 50 times more likely to progress to CKD than those not requiring renal replacement therapy. CRRT is a blood purification process that occurs over 24 hours within a critical care setting, whereas hemodialysis is an intermittent pro- cess occurring a few times a week. CRRT is preferred in patients with hemodynamic instability, cerebral edema, or severe hypovolemia. Peritoneal dialysis can be used alternatively, which may be better tolerated in some patients. Nutrition should provide adequate calories with restricted potassium and phosphate. KDIGO guide- lines for patients with AKI recommends a total energy intake of 20–30 kcal/kg per day. Minimal nitrogenous waste production is desirable in AKI; however, protein restriction is not recommended. Chronic Kidney Disease CDK is an irreversible, progressive disease process. Gradual in onset, the disease may develop over months to years, with 90% to 95% of the nephrons affected. CKD can progress to ESRD. In ESRD, kidney function deteriorates to the point that the kidney is unable to excrete waste products or control volume status, mak- ing dialysis or a kidney transplant the only options to support life. Epidemiology The incidence of CKD continues to increase in the United States. This increase is partially explained by the increase in the prevalence of DM and HTN, the two most common causes of CKD. It is estimated that almost 8% of adults 20 years old and older have some evidence of CKD based upon a severely reduced GFR. The highest incidence rate of ESRD occurs in older adults. The prevalence of CKD is 38% among patients older than 70 years. The incidence of CRF is signifi- cantly greater in the African American population, which may be attributed to increased HTN in this pop- ulation. A great number of genetic mutations have been discovered that correlate with increased predis- position to CKD. Genetic predisposition, secondary illness, lifestyle, and environmental factors all contrib- ute to the development of CKD. In the United States 37 million persons have CKD, which is approximately 7% of the population. Forty-eight percent of persons with severely reduced kidney function are unaware of their kidney disease. The mortality rate for patients with CKD is high; patients with late-stage CKD have more than a 75% mortality rate. Etiology There are numerous causes of CKD, with DM, HTN, glomerulonephritis, and ADPKD the leading etiologies (see Box 22-2).
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