560 UNIT VIII RENAL AND UROLOGICAL DISORDERS
Making the Connections—cont’d
Signs and Symptoms Treatment Goodpasture’s Syndrome (anti-GBM disease) | An autoimmune disease where the kidney nephrons and pulmonary alveolar membranes are attacked as an antigen. Assessment Findings Diagnostic Tests
Immunosuppressants. Plasmapheresis. Dialysis. Renal transplant.
Elevated serum creatinine, BUN, WBC count. Anti-GBM antibody titer (immunoassay and Western blot). ANCA titer. Chest x-ray shows bilateral hilar lymphadenopathy and diffuse consolidations. Urinalysis shows hematuria, proteinuria, and RBC casts. Pulmonary function test reveals restrictive disease.
Renal manifes- tations include hematuria, edema, and high blood pressure. Pulmo-
Malaise, chills, fever, dyspnea, pleuritic chest pain, cough, and hemoptysis. Massive pulmonary hemorrhage possible.
nary symptoms include tachy- pnea, cyanosis, and pulmonary crackles.
Acute Kidney Injury | Reversible failure of the kidneys caused by prerenal, intrinsic, or postrenal disorders. Prerenal AKI is most commonly renal ischemia caused by decreased blood volume. Intrinsic AKI is most commonly caused by nephrotoxic drugs, immune disorder, or infection. Postrenal AKI is most commonly caused by obstructive uropathy, as with nephrolithi- asis, prostate enlargement, or bladder disorders. Edema of the face and extremities. Oliguria. Fluid overload.
Diuretics. Cardiac monitor. Hemodialysis or CRRT in unstable patients.
Urinalysis, serum electrolytes, serum creatinine, BUN, arterial blood gases, and CBC. Calculate GFR. Radiographic imaging may be used to assess for any type of obstructive process or changes in size and structure of the kidneys. Renal biopsy may be used to evaluate for intrarenal etiology.
Edema in the face and extremities. Pulmonary edema can develop, causing respira- tory distress. Hypervolemia leads to HTN. Signs of uremia can develop, such as encephalop- athy, hyperkale- mia, metabolic acidosis, throm- bocytopenia, and neuromuscular irritability. As renal function returns, the patient demon- strates a diuresis phase, with urine output increasing to 1 to 2 liters per day and resolution of hypervolemia.
Lack of urine output initially. Dyspnea if pulmonary edema present. Confusion, sleepiness, stupor, or coma if nitrogenous wastes are high. Easy bruising if thrombocy- topenia develops. Fatigue, weakness, palpita- tions if anemia present. Muscle spasms possible if hypocalcemia present.
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