542 UNIT VIII RENAL AND UROLOGICAL DISORDERS
Regardless of mechanism, the antigen–antibody complexes damage the structure of the glomeruli and cause nephron dysfunction throughout the kidneys. Glomerular injury causes hyperpermeability of the capillaries, which allows loss of albumin and RBCs in the urine. The large loss of albumin from the blood- stream causes proteinuria, also called microalbumin- uria. Because albumin content of the bloodstream decreases, diminished colloid oncotic pressure (COP) occurs throughout the body. According to Starling’s Law of Capillary Forces, the decrease of COP causes an imbalance in hydrostatic and oncotic pressure. The low COP is overcome by hydrostatic pressure, which causes edema. Also, because glomerular filtration of the blood is diminished, urine production is also diminished. As GFR decreases, oliguria , which is lack of sufficient urine production, develops. The patient becomes hypervolemic and edematous, and blood pressure rises. CLINICAL CONCEPT A certain amount of urine production is necessary to excrete waste products. An inadequate amount of urine is termed oliguria. Oliguria is defined as less than 400 mL of urine output per day or less than 20 mL of urine per hour. Clinical Presentation Acute glomerulonephritis has a classic presentation of sudden edema (most prevalent in the periorbital region), hematuria, proteinuria, oliguria, and HTN. The onset of clinical manifestations occurs approx- imately 7 to 21 days following a streptococcal infec- tion. This is consistent with the time frame needed for antibody formation. As glomerular function decreases, urinary output decreases. As glomerular injury increases, hematuria and proteinuria increase. The patient develops puffiness of the eyelids and facial edema. The urine is dark because it contains RBCs; it has been described as cola-colored. Blood pressure is often ele- vated. Nonspecific symptoms include weakness, fever, abdominal pain, and malaise. The patient may com- plain of CVA tenderness.
metabolic panel are necessary. Serum creatinine and BUN will be modestly elevated in PSGN. Mild ane- mia is common in the early stages due to decreased erythropoietin secretion. Serum complement levels C3 and C4 are low as they are used up by the forma- tion of immune complexes deposited in the glomeru- lar membranes. Hypoproteinemia is often present due to loss of protein in the urine (proteinuria). A 24-hour urine protein quantification is necessary. Serum electrolytes are usually normal. Urine studies will show a large amount of protein, WBCs, and blood in the urine with hyaline or cellular casts. Urine creat- inine clearance will be low because dysfunctional kidneys do not excrete nitrogenous wastes. Creati- nine accumulates in the blood. Serum albumin will be low as it is filtered out of the permeable, inflamed glomerulus. Hepatitis B and C and HIV serology testing are necessary. The streptozyme test is used to measure five different types of antistreptococ- cal antibodies: antistreptolysin O, antihyaluronidase (AHase), antistreptokinase (ASKase), antinicotinamide– adenine dinucleotidase (anti-NAD), and antiDNAse B antibodies. Blood tests for antineutrophil cytoplasmic antibodies (ANCA), anti–double-stranded DNA anti- body, and antiglomerular basement membrane (GBM) serology are done to rule out causes of rapidly pro- gressing AGN. Imaging studies do not provide valuable diagnostic information. Treatment The management of AGN is based largely upon clini- cal presentation and symptoms. Antibiotics are neces- sary if the etiology is poststreptococcal infection. The treatment of glomerulonephritis associated with an active infection is aimed at eradication of the current infection. Antipyretics and analgesics are also needed. If HTN is present, antihypertensive medication is nec- essary. If edema is present, diuretics may be indicated. Dietary restrictions of sodium and protein are also advised. IgA Nephropathy IgA nephropathy is one of the most common forms of glomerulonephritis. There are geographical differ- ences in the incidence of this disease across the world. There is a 30% prevalence in Asia and the Pacific Rim, 20% prevalence in Southern Europe, and much lower prevalence in Northern Europe and North America. There is a male preponderance with peak incidence in the second and third decade of life. The most common clinical presentation includes hematuria, often after a respiratory infection accompanied by proteinuria. The majority of patients have benign disease with complete remission. However, IgA nephropathy can have a rapidly progressive course to renal failure. Deposits of IgA, either alone or with IgG, IgM, and complement protein, are found in the glomerular region of the nephrons. There is andinflammatory
CLINICAL CONCEPT Point tenderness over the flank and CVA tenderness is a classic symptom of kidney infection.
Diagnosis The gold standard for diagnosing glomerulonephritis is a kidney biopsy, with hallmark glomerular inflam- mation characterized by increased glomerular cel- lularity. However, the diagnosis is most often made on a clinical basis without biopsy. CBC and complete
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