UNIT NINE
706
Understanding the Urinary System
structures. The cysts are grapelike and contain serous fluid, blood, or urine. The patient typically first shows signs of the disease in adulthood. The initial symptoms include a dull heaviness in the flank or lumbar region and hematuria. Other symptoms include hypertension and UTIs. The renal cysts are diagnosed with ultrasound imaging. Treatment includes antihypertensive medications, dietary sodium restriction, and daily fluid intake of more than 3 liters. There is no treat- ment to stop the progression of polycystic kidney disease. As the disease progresses, the patient will likely develop CKD (discussed later) and require kidney replacement ther- apy. Because polycystic kidney disease is hereditary, patients should be offered genetic counseling.
Diagnostic Tests Diabetic nephropathy is diagnosed by monitoring the patient with diabetes for onset of albuminuria or protein spillage in the urine, an early sign of the disease. A kidney biopsy may be done. Therapeutic Measures In the early stages of diabetic nephropathy, strict control of blood glucose levels (A1C less than 7%) and blood pres- sure helps slow the progress of the disease and reduce symp- toms. Angiotensin-converting enzyme (ACE) inhibitors or angiotensin II receptor blockers (ARBs) are prescribed for hypertension. Statins are prescribed for cholesterol and pro- teinuria reduction. A healthy lifestyle should be encouraged to help manage this disease. As the disease progresses, kid- ney replacement therapy (dialysis or kidney transplant) may be needed. Nephrotic Syndrome Nephrotic syndrome is the excretion of 3.5 grams or more of protein in the urine per day. In nephrotic syndrome, large amounts of protein are lost in the urine from increased glo- merular membrane permeability. As a result, serum albumin and total serum protein are decreased. Normally, albumin and other serum proteins maintain fluid within the vascular space. When levels of these proteins are low, fluid leaks from the blood vessels into tissues, resulting in edema. With very low levels of protein, ascites and massive widespread edema (anasarca) occur. In response to the low protein levels, the liver produces lipoproteins. As a result, serum cholesterol, low-density lipoproteins, and triglyceride levels are ele- vated. Urine may appear foamy from lipoproteinemia. Loss of immunoglobulins may lead to increased susceptibility to infection. Acute kidney injury, endocrine dysfunction, and thrombotic disease can occur. Complications of nephrotic syndrome include impaired immune function, protein imbalances, and most important, increased blood coagulation. The latter is due to urinary loss of clotting inhibitors such as antithrombin III and plasmino- gen along with the loss of protein. Treatment is focused on the cause and symptoms of nephrotic syndrome. ACE inhibitors or ARBs are prescribed to reduce pressure in the glomerulus and slow protein excre- tion. To reduce edema, loop diuretics and sodium intake restriction (2 grams/day) are used. Protein intake is guided by the severity of urinary protein loss. Statins to lower lip- ids may be tried. Anticoagulants are given for thrombosis prevention. In some cases, corticosteroids may be used to reduce inflammation. Nursing care focuses on edema, protein intake, and prevent- ing infection. For edema, daily weights, careful I&O measure- ments, and abdominal girth measurements are documented.
CHRONIC RENAL DISEASES
Diabetic Nephropathy Diabetes is the most common cause of CKD and end-stage kidney disease. Diabetic nephropathy , one type of diabetic kidney disease, is caused by years of damage from elevated glucose levels to the small blood vessels in the kidneys. Risk factors for diabetic nephropathy include chronic hyperglyce- mia, hypertension, high cholesterol, genetic predisposition, and smoking. Careful control of blood glucose levels, hyper- tension, and weight; not smoking; and careful use or avoid- ance of NSAIDs reduces the risk of nephropathy in patients with diabetes. Pathophysiology Multiple factors contribute to diabetic nephropathy. It begins with increased osmotic pressure from hyperglyce- mia, increased diuresis and compensatory cell growth and expansion, and increased glomerular filtration rate (GFR). Widespread atherosclerotic changes occur in the blood ves- sels of patients with diabetes, decreasing the blood supply to the kidney. Abnormal thickening of glomerular capillaries damages the glomerulus, allowing protein to leak into urine. Patients with diabetes also commonly develop pyelonephri- tis and renal scarring. Another complication of diabetes, neurogenic bladder, causes incomplete bladder emptying. This results in urine retention, which can cause infection, further damaging the kidneys. The patient can lose large amounts of protein (e.g., albumin) in the urine and develop nephrotic syndrome. This causes massive edema because of the resultant low levels of albumin in the blood. Symptoms The progression of nephropathy is marked by persistently elevated albuminuria advancing to proteinuria. Hypertension accelerates renal damage. As diabetic nephropathy pro- gresses, GFR decreases, waste products accumulate, and eventually the patient may develop CKD. Complications The risk of cardiovascular disease is significant as protein spilling in the urine progresses.
• WORD • BUILDING • nephropathy: nephro—pertaining to the kidney + pathy—disease
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