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RENAL UNIT CASE 11 |
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Clinical History: J.C., a 55-year-old man, had been followed for many years for a variety of problems including insulin dependent diabetes mellitus for 13 years, coronary artery disease with angina for 8 years and a myocardial infarction three years ago, chronic bronchitis and occasional ethanol withdrawal symptoms. On June 8, 1973 he came to the Emergency Room complaining of flank pain and dysuria. There was tenderness to percussion in the costovertebral angles. Urinalysis: pH 6.5, glucose 1+, protein 2+, Sp. Gr. 1.012. The sediment was loaded with WBC and a gram stain of the unspun sediment showed gram negative rods. A culture of the urine subsequently grew E. Coli and Proteus Mirabilia. He was treated with antibiotics and subsequent cultures were negative. Creatinine at a follow-up in July 1973 was 1.1 mg/dl. He had a few similar episodes and in April 1974 he had edema and 4+ proteinuria. The 24 hour urinary excretion of protein was 5.2 gram and the serum albumin was 2.4 g/dl. In October of 1974 he had another episode of urinary infection and he complained that he had to urinate small volumes frequently and he occasionally dribbled urine involuntarily. Rectal examination revealed no prostate enlargement. Blood pressure and serum creatinine measures summarized from chart: Date: 7/73 10/73 1/74 6/74 9/74 10/74 Creatinine: 1.1 1.2 1.4 1.8 2.4 6.5 B.P.: 140/90 150/95 150/95 160/95 155/100 150/100 mmHg Questions: 1. What are the ways in which urinary tract function may have been impaired as a consequence of his systemic diseases? Correlate with the clinical findings in this case. Figure 1 is from the urine sediment. What does it show? 2. Is the patient's course consistent with simple progression of chronic renal disease? 3. In October 1974 a retrograde pyelogram was done. These films are not available but they were similar to what is shown in Figure 2. What is your interpretation? (Not all clinicians would agree that this procedure was appropriate, but he tolerated it well and we can learn from the findings). 4. Is nephrotic syndrome common in diabetes? What does its presence indicate in regard to prognosis? 5. What is the evidence that the glomerular lesions in diabetes are a consequence of the metabolic disorders? 6. This patient died in 1976. One kidney is shown in Figure 3. 7. Figures 4 (A&B) and Figure 5 show its microscopic appearance (H&E). Figure 6 shows the electron microscopy: The distance between the two black lines in the EM is normal GBM thickness. |
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