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RENAL UNIT CASE 10 |
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Clinical History: A 19 year old married, red haired female developed a skin eruption involving the malar areas of the face, neck and arms. She had no major illnesses in the past. However, seven months previously she had a spontaneous abortion. Following the appearance of the rash, she developed intermittently blurred vision. On two occasions her husband observed that she was behaving strangely, talking to herself and apparently seeing non-existent people. These episodes were brief and seemed to go away by themselves. She was initially seen in OB/GYN clinic with BP of 135/90 mm Hg and a pulse of 105/min. She weighed 15 pounds more than on the previous clinic visit. Her abdomen contained fluid and she had periorbital and pedal edema. The skin eruption was still present. A few fine rales were heard in the lungs. A chest X-ray showed blunting of the costophrenic angles. Serum creatinine was 2.1 mg/dl, BUN 32 mg/dl, albumin 2.8 g/dl, C3 not detectable; ANA positive in dilution of 1:320, Hct 30%. Questions: 1. What do the clinical and laboratory data tell you about this case? Consider organs involved, clinical patterns of renal disease, pathogenic mechanisms, diagnosis, pathophysiology, etc.? What additional data do you want? 2. What would you expect to find in the urinalysis? 3. Why might a biopsy be done in this case? 4. Figure 1 and Figure 2 are representative of all the glomeruli. What would the significance be if only 30% had this appearance and the remainder were normal or minimally abnormal? 5. Figure 3 shows immunofluorescence for IgG. Stains for IgA, IgM and C3 were similar. Figure 4 shows electron microscopy. What do these say about pathogenesis, management and prognosis? 6. In another case of the same disease all glomeruli appeared as in Figures 5, Figure 6, Figure 7(a & b). Compare these with the previous ones. Would you expect a similar clinical picture and prognosis? 7. The originally described patient was treated with Prednisone, and Cytoxan. Over the next 6 months all symptoms and signs disappeared except for proteinuria and mild edema. The serum creatinine fell to 1.1 mg/dl and the serum C3 level was 90% of normal. A second biopsy was done 14 months after the first. All glomeruli looked like the ones in Figures 8(a & b), Figure 9 and Figure 10. What has happened at the structural level? 8. What do you know about the pathogenesis of this disease? Can you explain why it has so many different kinds of renal pathology? How can you use your knowledge of pathogenetic mechanisms to follow the course of the disease clinically? |
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