558 UNIT VIII RENAL AND UROLOGICAL DISORDERS
• Creatinine clearance, the volume of blood plasma cleared of creatinine per unit time, can also be used to gauge kidney function. • BUN should not be used alone to gauge kidney function as it rises in dehydration and high-protein diets. • Oliguria is less than 400 mL of urine output per day. • In acute postinfectious glomerulonephritis, an immu- nological reaction triggers inflammation that damages the membranes of the glomerulus. • Nephrotic syndrome is caused by glomerular injury and causes hypoalbuminemia, edema, and proteinuria. Hyperlipidemia and HTN are also associated with the syndrome. • Anti-GBM disease is autoimmune destruction of the glomerulus and is commonly part of Goodpasture’s syndrome, which also involves autoimmune disease of the lungs. • Pyelonephritis is an infection of the kidney that causes fever, chills, and CVA tenderness. • An anatomical abnormality called vesicoureteral reflux is a common predisposing factor for pyelone- phritis. Reflux of urine occurs from the bladder into the ureter.
• Nephrolithiasis causes colicky pain in the back radiating to the groin, hematuria, and crystalluria. • The most common type of kidney stone is made of calcium oxalate. • Hydronephrosis is swelling of the renal pelvis that can occur with obstructive uropathy. • AKI is most often caused by ischemia of the kidney, which is reversible. • DM and HTN are the most common causes of CKD. • CKD is irreversible and categorized into five stages according to serum creatinine and GFR. • CKD causes widespread systemic symptoms such as hypervolemia, encephalopathy, thrombocytopenia, anemia, HTN, metabolic acidosis, hyperparathyroidism with renal osteodystrophy, peripheral and autonomic neuropathy, hyperkalemia, azotemia, impaired glucose metabolism, hypocalcemia, and hyperphosphatemia. CKD can lead to heart failure, left ventricular hypertro- phy, pulmonary edema, and uremic pericarditis. • ESRD occurs when there is 5% to 10% nephron function. • Hemodialysis is most often used to treat ESRD. Kidney transplant is the only treatment that leads to complete rehabilitation.
Making the Connections
Pathophysiology
Signs and Symptoms Treatment Glomerulonephritis | Most commonly caused by GABHS antibodies that develop against the antigen (strep); for unknown reasons, antibodies attack glomerular membranes (molecular mimicry theory). Another theory asserts that antigen– antibody complexes develop and deposit in glomerular membranes, causing inflammation. Back pain (CVA tenderness). Edema (commonly periorbital). Fever. Cola-colored urine. Malaise. HTN. Assessment Findings Diagnostic Tests Proteinuria. Hematuria. Edema (periorbital region common).
Antibiotics, antipyretics, and analgesics are needed. With systematic manifesta- tions such as edema and elevated blood pressure, diuretics and antihypertensive agents may be indicated. Dietary restrictions of sodium and protein are also advised.
Elevated serum creatinine and elevated BUN. Urinalysis shows a large amount of protein and blood. Urine 24-hour creatinine clearance is low because creatinine is not being filtered by dysfunctional kidneys. Streptolysin antibody titer demon- strates antibodies are present against GABHS. Cryoglobulin titer indicates antigen–antibody complexes are present. Complement in the blood is low and is depleted because immune reaction uses up complement. Blood tests for antineutrophil cytoplasmic antibodies (ANCA), antidouble stranded DNA antibody, and antiglomerular basement membrane (GBM) serology are done to rule out causes of rapidly progressive AGN.
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