CHAPTER 22 Renal Disorders 543
type of hypercellularity with destruction of capillar- ies and fibrosis of the nephron tubules. Angiotensin- converting enzyme inhibitors, corticosteroids, and immunosuppressants have been effective in some patients. Plasmapheresis, a procedure that removes the antibodies from the plasma portion of the blood- stream, has also been used for some patients. Nephrotic Syndrome Nephrotic syndrome is a combination of clinical findings that occurs when the glomeruli are damaged. When glomeruli are injured, they become hyperper- meable to proteins and other substances in the blood- stream. The blood becomes depleted of albumin and other large molecules as they enter into the nephron tubules and become excreted with the urine. Epidemiology Diabetic nephropathy is the most common type of nephrotic syndrome, with an incidence of 50 to 100 cases per million population per year. Native Ameri- cans, Latino Americans, and African Americans have a higher incidence than do European Americans. There is a male predominance in the occurrence of nephrotic syndrome, as there is for CKD in general. However, nephrotic syndrome secondary to SLE is more com- mon in women. Etiology Three systemic diseases—DM, amyloidosis, and SLE—are implicated in more than 90% of all cases of nephrotic syndrome in adults. Other causes include immune-complex deposition disease, vasculitis, allergies, preeclampsia, morbid obesity, malignant HTN, and infections such as bacterial endocarditis and tuberculosis. In children, 70% to 90% of cases of nephrotic syndrome is caused by minimal change dis- ease (MCD) which is associated with edema, severe hypoalbuminemia, and massive proteinuria. The cause of MCD is unknown. Pathophysiology Glomerular damage occurs either as a primary insult or secondary to one of the causes described. Structural changes that occur in the glomerulus include injury to the endothelial cells, derangement of the basement membrane, and damage to the epithelium. Massive albuminuria (also called proteinuria ) is a conse- quence of the glomerular damage. As albumin is lost in the vascular space, edema forms because of decreased colloidal osmotic pressure. Clinical Presentation Patients have albuminuria with consequent edema. Facial edema is common, especially in the periorbital region. With severe albumin loss, edema of the lower extremities, pleural effusion, and ascites can develop. Patients also often present with hematuria and HTN.
Diagnosis The work-up for nephrotic syndrome includes uri- nalysis and blood tests for albumin, BUN, and serum creatinine. Urinalysis usually shows proteinuria and hematuria. Elevations in BUN and serum creatinine occur and are followed to assess renal function. The serum albumin level is classically low in nephrotic syndrome, below its normal range of 3.5 to 4.5 g/dL. Tests for hepatitis B and C, HIV, and lupus, including antinuclear antibody (ANA), anti–double-stranded DNA (antidsDNA) antibodies, and complement, are commonly done when the etiology of nephrotic syn- drome is unclear. In immunological etiologies of nephrotic syndrome, complement in the bloodstream is decreased. A 24-hour urine sample is collected for analysis. The urine can contain up to 3 grams of protein over 24 hours (normal is fewer than 150 mg/day). The urine also contains fatty casts caused by loss of lipoproteins at the glomerulus, which take on the shape of the tubules before excretion into urine. Renal ultrasonog- raphy and renal biopsy may be done when etiology is unclear. Treatment The patient with nephrotic syndrome needs to be vigilant of nutritional needs. The diet should provide adequate energy (caloric) intake and adequate protein (1 to 2 g/kg/d). However, supplemental dietary protein is of no proven value because it will be excreted. A low-sodium diet (fewer than 1500 g/day) will help to limit fluid overload. Adequate fluid intake is essential, but overhydration should be avoided. Because albumin levels are low, it is important to recognize that there are fewer binding sites for drugs. This will increase the amount of free active drug in the bloodstream. Also in nephrotic syndrome, immu- noglobulins are lost to the urine. This increases sus- ceptibility to infection. Pneumococcal and influenza vaccines should be administered to protect the patient from infection. Angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) are used to lower blood pressure. They also slow the progression of kidney disease. Complications As nephrotic syndrome progresses, hyperlipidemia may develop secondary to increased lipoprotein syn- thesis in the liver. As the liver increases synthesis of albumin to replenish the lost albumin in the urine, it also hypersynthesizes lipids. There is commonly an elevation in low-density lipoprotein (LDL) and triglycerides. Hyperlipidemia requires drugs such as statins that decrease liver synthesis of lipids. With increased loss of protein in the urine, there is loss of antithrombin III and plasminogen, the body’s natural thrombolytic substances. This increases the risk of thromboembolism, and patients may require antico- agulants (see Fig. 22-8).
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