Urological complications in renal transplantation.
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Biomedical subjects
Publications and source records attributed to P Michielsen.
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A 23-year-old multiparous normotensive woman developed a hemolytic uremic syndrome (HUS) five months postpartum, and four months after starting estro-progestogen contraception. Eight years later a recurrence appeared, five years after a successful cadaver kidney transplantation and ten months after resumption of the estro-progestogen intake. In the interval a pure progestogen contraceptive was prescribed without problems. This observation is consistent with the hypothesis that HUS can be triggered by oral estrogen intake in predisposed individuals.
A 37-year-old white male, working in a tile factory, presented proteinuria with no obvious tubular dysfunctional. Renal biopsy disclosed a mild focal segmental proliferative glomerulonephritis. Distinct alterations were found by electron microscopy, especially in the proximal tubular cells. Because of a history of heavy dust exposure the silicon content was determined in the kidney biopsy tissue. The finding of 150 mg/kg silicon on tissue dry weight supports the diagnosis of silicon nephropathy.
Lymphocele and lymphatic fistulae are relatively benign complications in renal transplantation. The incidence in our series of 248 renal transplants was 8%. The origin and pathogenesis of lymph collection and augmented lymph flow are discussed. The main importance of this complication lies in its differential diagnosis with urinary fistula and acute rejection episode or deep phlebothrombosis with all its therapeutic implications. Important lymph accumulations should be drained. We prefer as initial treatment a percutaneous closed aspiration which most successfully solves the problem. In case this method should fail, one can choose between external or internal drainage. As in literature, we actually prefer an internal marsupialisation, but completed by an omentoplasty if the leakage originates from the kidney.
A 34-year-old male is reported with carpal and tarsal osteolysis syndrome. In addition he presented a fluctuating proteinuria and a slightly reduced renal function. The relevant literature on the subject is reviewed and the combination of carpal and tarsal osteolysis with nephropathy is discussed.
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A patient who developed a lymphocele five years after renal transplantation is presented and discussed.
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During treatment with indomethacin in a patient with Bartter's syndrome, hypokalemia, high plasma renin concentration, hyperaldosteronism and decreased sensitivity to angiotensin infusion were corrected. A particular finding in the renal biopsy specimen was a marked hyperplasia of renomedullary interstitial cells which had characteristics similar to the cells known to produce renal prostaglandins. The hypothesis is formultated that the primary defect in this syndrome is related to hyperplasia of renomedullary interstitial cells and inappropriate release of renal prostaglandins giving rise to decreased sodium reabsorption, volume depletion and hypersecretion of renin and aldosterone.
This paper describes the clinical history of two male nontwin siblings with late-onset cystinosis, a variant of cystine storage disease. The diagnosis was established clinically and confirmed by measurement of cystine concentrations in leucocytes and skin-fibroblasts. Both patients presented with an incomplete nephrotic syndrome and renal biopsy showed, in addition to lesions of polykaryocytosis, a picture of focal and segmental glomerular hyalinosis. Renal function was stable in one patient over a follow-up period of two years; the other patient progressed toward terminal renal failure and was successfully transplanted.
189 patients with various types of glomerular disease were studied. Creatinine clearance, protein excretion and urinary excretion of fibrin degradation products (FDPs) were measured before and at various intervals (up to 42 months) after starting treatment with indomethacin, alone or in combination with other drugs. The following observations were made: a. Patients with a urinary FDP in excess of 2 mg/24 hours before treatment had a significantly lower creatinine clearance and a significantly higher protein excretion than patients excreting less than 2 mg FDP/24 hours, indicating that FDP excretion reflects the severity of the renal disease. b. During treatment, the incidence of high FDP excretion decreases progressively, but remains high in patients who ultimately develop renal insufficiency. c. There is no correlation between the initial value of FDP excretion and the subsequent changes in creatinine clearance and proteinuria during treatment. This implies either that the initial FDP excretion has no prognostic value or, perhaps more likely, that disease activity is modified by treatment. d. The best correlation between FDP excretion and evolution is found in proliferative glomerulonephritis. There are reason to suppose that, in this group at least, the treatment influenced the evolution of the disease.
33 cases of chronic glomerulonephritis who responded unsatisfactorily to treatment with indomethacin alone were treated in addition with a low dose of cyclophosphamide. The five patients with focal glomerulosclerosis responded poorly. The remaining 28 patients showed a statistically significant improvement in renal function and proteinuria.
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Indomethacin given to adults with glomerulonephritis usually reduces their urinary excretion of protein and fibrinogen/fibrin-related (F.R.) antigen. Nevertheless, non-responders exist. Platelet aggregation is significantly more strongly inhibited by indomethacin in good responders than in nonresponders. This supports the hypothesis that the reduction of urinary excretion of F.R. antigen during indomethacin administration is related, at least in part, to inhibition of intrarenal platelet aggregation and of the subsequent fibrin deposition.
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