CLINICAL PRESENTATION
Renal insufficiency results in signs and symptoms that reflect loss of the regulatory, excretory,and endocrine functions of the kidney. The inability to regulate the volume of body fluid compartments may be expressed as edema, hypertension, or congestive heart failure. The loss of ability to regulate the composition of the body fluids is evidenced by the development of hyperkalemia, metabolic acidosis, and hyperphosphatemia.
The loss of excretory ability of the kidney is expressed by a rise in the plasma concentration of specific substances normally excreted by the kidney. The most widely monitored indices are the blood urea nitrogen (BUN) and concentration of creatinine in the serum. The rate of rise of BUN and creatinine reflects the impairment in the filtration function of the kidney and the rate of generation of urea nitrogen and creatinine. Creatinine generation is proportional to muscle mass. Accordingly, a patient with acute renal failure and a large mass of muscle may have an increase in the serum concentration of creatinine of several milligrams per deciliter per day. A patient with smaller initial muscle mass but with the same degree of renal filtration failure may have a slower rate of rise. Urea nitrogen derives from the catab-olism of protein. In a catabolic patient, blood urea nitrogen may increase by over 40 mg/dl/day. In a patient who is not catabolic and in whom the dietary intake of protein is low, the rate of urea nitrogen generation will be less and the blood level will increase at a slower rate. Thus, while increases in the serum concentration of urea nitrogen and creatinine indicate the presence of renal disease, the absolute blood concentrations obtained and the rate of change are related to both the degree of renal injury and the rate of generation. A thin, elderly individual can be severely and symptomatically uremic despite the fact that the serum concentration of creatinine is only 2 mg/dl. Conversely, such a value would be only modestly abnormal in a young, muscular, athletic person.
- Esophagogastroduodenoscopy
- Sickle Cell Anemia (SS)
- DEFINITION
- PATHOPHYSIOLOGY OF AIRWAY OBSTRUCTION
- Gardner's Syndrome
- ACUTE AND CHRONIC HEPATITIS - DEFIRILTIORI
- APPROACH TO THE PATIENT WJTH SUSPECTED MALDIGESTION AND/OR MALABSORPTION
- Minimal Change Nephropathy
- Laparoscopy
- GASTRITIS
- BILIRUBIN METABOLISM
- Texas MedicareRX
- CLINICAL PRESENTATION AND DIAGNOSIS
- TREATMENT
- LIVER ABSCESS
- ETIOLOGY
- Therapy
- PATHOPHYSIOLOGY OF ISCHEMIC HEART DISEASE
- Mechanism of Proteinuria
- EMBOLIC DISEASE
- COMPLICATIONS OF MYOCARDIAL INFARCTION AND THEIR MANAGEMENT
- Renal Biopsy and Other Diagnostic Tests
- Public health and environment
- CARCINOMA OF THE COLON
- Restrictive Cardiomyopathy
- Specific Etiologies
- CARCINOMA OF THE PANCREAS - Diagnosis
- NONATHEROSCLEROTIC CAUSES OF CORONARY ARTERY OBSTRUCTION
- PHYSIOLOGY OF THE CORONARY CIRCULATION
- Miscellaneous
- Renal Tumors
- Conjugated Hyperbilirubinemia
- Treatment and Prognosis
- THE FAMILIAL POLYPOSIS SYNDROMES
- CARDIAC DEVELOPMENT