Search

Treatment with acetazolamide for pseudotumor cerebri (PTC) in a renal transplant patient led to an acute, but reversible deterioration in renal function. Possible pathogenetic mechanisms behind acute renal failure and acetazolamide are detailed. In summary, caution should be exercised in all patients with chronic renal failure who require acetazolamide. It should be avoided if possible, used in reduced doses when necessary, and coupled with a high fluid intake to avoid dehydration and/or intraluminal obstruction.

A 35-year-old renal transplant patient with stable renal function developed an unexplained anaemia. Appropriate investigations proved non-diagnostic. Only when enalapril therapy was stopped did the anaemia reverse and haemoglobin levels returned to pre-treatment levels. An association between angiotensin-converting enzyme inhibitors and anaemia in patients with renal failure is becoming more evident. A literature review of this problem and its possible pathogenesis in patients with renal failure is given.

Cyclosporine has been shown to reduce renal perfusion and to decrease glomerular filtration rate. Experimental studies suggest that nifedipine might reverse this renal vasoconstrictive effect of cyclosporine. We studied renal hemodynamics of 5 cyclosporine-treated renal transplant recipients before and after 2 weeks of therapy with high-dose nifedipine (up to 120 mg/day). Pretreatment GFR and renal plasma flow (RPF) were decreased. Following administration of nifedipine, RPF increased by 18% (P less than 0.01), while GFR did not change. Filtration fraction decreased by 10.5% (P less than 0.01). Mean arterial pressure declined from 111 +/- 5 to 96 +/- 3 mmHg (P less than 0.01). Renal vascular resistance dropped by 25% (P less than 0.01). Calculated postglomerular plasma flow increased by 20.5% (P less than 0.01). Urinary albumin excretion rate was unaffected. Cyclosporine whole blood levels were unchanged. The increase in RPF and in postglomerular plasma flow suggests that high-dose nifedipine might lessen cyclosporine-induced glomerular and interstitial ischemia in renal allograft recipients.

We describe a patient with clinical signs of mixed connective tissue disease who developed nephrotic syndrome. The kidney biopsy revealed glomerular and vascular deposits that stained positive with Congo red and showed a green birefringence. The Congo red positivity became negative in sections treated with potassium permanganate. Peroxidase-antiperoxidase staining with anti-AA antibodies was strongly positive. Ultrastructurally, although the deposits were similar to amyloid, they were about twice the size of amyloid fibrils. To our knowledge, the deposition of an amyloidlike material that shows the histochemical and immunohistochemical features of amyloid AA but is lacking the distinctive ultrastructural characteristics of amyloid fibrils has not been described.

Accepted criteria for the diagnosis of peritonitis in CAPD include: 1. symptoms and signs of peritoneal irritation; 2. a cloudy effluent with white blood cell (WBC) count greater than 100/microliters and; 3. a positive culture. In fact, the earliest suggestive sign of peritonitis is a turbid effluent. However, symptomatology of peritoneal irritation may precede the development of a cloudy fluid. We hereby report on two CAPD patients with culture proven peritonitis whose initial presentation was that of an acute abdomen. Although diffuse rebound tenderness was elicited the initial effluent, after an overnight dwell, was clear with a WBC count of 80 and 70/microliters, respectively. Working diagnoses on admission included a ruptured cyst and a perforated peptic ulcer. Both patients were in line for a laparotomy. After a period of 7 and 12 hours, respectively the ensuing effluents turned turbid with WBC counts of 6,400 and 2,500/microliters. Cultures eventually grew Staphylococcus aureus and Streptococcus viridans. Appropriate antibiotic treatment resulted in full recovery.

The element content of the fingernails of 16 patients with chronic renal failure (CRF) treated by hemodialysis was examined by dispersive microanalysis. In comparison with matched controls, the results showed a statistically significant decrease in the percentage of Cu, Fe and Zn and an increase in S. The Al content did not differ significantly from that of the controls. There was no correlation between the serum values of Al, Fe and Zn and their content in the fingernails of the patients. On the other hand, Cu was found to be low both in the sera and in the fingernails of the CRF patients.

DNA repair following ultraviolet (UV)-induced DNA damage is decreased in some cancer-prone diseases. Cancer frequency in end-stage renal disease patients is higher than in the normal population. Therefore, DNA repair from UV-induced damage in lymphocytes was determined in 11 hemodialysis (HD) patients, 11 patients on continuous ambulatory peritoneal dialysis (CAPD), 10 patients with chronic renal failure (CRF) who had not yet been dialyzed and in 12 controls. UV irradiation at 254 nm was followed by 3H-thymidine incorporation in the presence of hydroxyurea. DNA repair synthesis in CAPD and CRF was significantly reduced to only 69 and 54% of the control, respectively, whereas the repair of HD patients was close to normal (86%, p = n.s.). The impaired ability to correct DNA damage may contribute to the increased cancer incidence in uremic patients.

Two cases of subclavian vein stenosis secondary to permanent cardiac pacemakers are presented. Both stenoses were asymptomatic until arteriovenous fistulae/grafts were constructed in order to initiate haemodialysis. One patient experienced severe oedema of the arm which necessitated surgical closure of the graft. A literature review into major venous stenosis and cardiac pacemakers reveals an asymptomatic, but evidently underestimated, problem. As more elderly patients will be accepted onto haemodialysis programmes, this above-mentioned problem may become more common. Therapeutic answers as to haemodialysis access are discussed in these patients with permanent pacemakers who need haemodialysis.

A 45-year-old woman on CAPD developed pneumococcal peritonitis. This is the second such case of Streptococcus pneumoniae peritonitis complicating CAPD. The role of an indwelling intrauterine device (IUD) in producing ascending infection into the peritoneum is discussed, especially in women with evidence of retrograde menstruation. A review of the literature concerning pneumococcal peritonitis associated with IUD is given. Possible contraception to women on CAPD is briefly mentioned.

Successful pregnancies in women on regular hemodialysis treatment are infrequent but increasing. We present two such cases; both pregnancies were diagnosed early, and hemodialysis was intensified, leading to significant reductions in predialysis serum urea levels (70-100 mg/dl). One case was particularly unusual in that systemic lupus erythematosus was the underlying disease, and the patient had no residual renal function at the time of conception. Both patients delivered by cesarean section at 32 and 35 weeks, and their infants are well at ages 2 years and 18 months, respectively. The management and the complications associated with such pregnancies are discussed.

We report a 24-year-old woman on chronic hemodialysis for 7 years in whom investigations for an acute hearing loss revealed a serous otitis media. Tissue obtained at bilateral tympanotomy contained amyloid, which proved to be sensitive to potassium permanganate. This finding may indicate that amyloidosis in hemodialyzed patients is more common than initially thought. A brief review of amyloidosis in hemodialyzed patients is given.

The histopathological changes in the livers of 11 patients treated with alkylated and nonalkylated anabolic androgenic steroids are presented. The histological changes in the liver included: proliferation of the bile ducts with or without cystic dilatation (9/11), peliosis (8/11), atypical hyperplasia of liver cells (2/11), and tumors (3/11). The latter included one case of cholangiocarcinoma, one of hepatocellular carcinoma, and one of combined cholangiocellular and hepatocellular carcinoma. The pathological changes in the liver in this series suggest a possible relationship between anabolic androgenic steroids and bile duct proliferation and/or cholangiocarcinoma.

The effect of 30% Urografin on platelet aggregation induced by adenosine diphosphate (ADP), epinephrine, and arachidonic acid was examined. In vivo and in vitro experiments in 10 nondiabetic subjects and in vitro experiments in 7 diabetic-uremic patients showed a statistically significant decrease in platelet aggregation 20 minutes after in vitro incubation or in vivo infusion with Urografin. Urografin concentration was about 2.4-2.5%. The possibility of bleeding induced by contrast media and the connection with acute renal failure in diabetic-uremic patients are discussed.

Deterioration of renal function after acute bacterial pyelonephritis is rare. We report on 2 patients with a solitary functioning kidney in whom acute renal failure developed in the setting of acute bacterial pyelonephritis. Following antimicrobial treatment kidney function returned to baseline values. This finding suggests that patients with a solitary functioning kidney are more prone to have renal dysfunction after acute bacterial pyelonephritis.

The case of a 40-year-old patient who underwent an unsuccessful cadaver kidney transplantation and was treated with ethambutol and isoniazid is reported. A bilateral retrobulbar neuropathy with an unusual central bitemporal hemianopic scotoma was found. Ethambutol was stopped and only small improvement of the visual acuity followed. Isoniazid was discontinued later, followed by a dramatic improvement in the visual acuity. The hazards of optic nerve toxicity due to ethambutol are known. We emphasize the potential danger in the use of ethambutol and isoniazid.

A pathogenetic role of secondary hyperparathyroidism in the anemia of chronic renal failure has been suggested. To investigate this relationship, the biochemical factors of secondary hyperparathyroidism (calcium, phosphorus, alkaline phosphatase, and immunoreactive parathyroid hormone) were correlated with hematocrit levels in 96 long-term hemodialysis patients. We also compared hematocrit values before and after parathyroidectomy in 18 patients. No correlation between hematocrit level and biochemical indices of secondary hyperparathyroidism could be found. However, in 44% of the patients with parathyroidectomies, the hematocrit reading increased after surgery. The importance and possible cause of this improvement of anemia in this group is discussed.

Six of 102 patients with end-stage renal disease (ESRD) who underwent hemodialysis treatment from 1972 to 1980 developed active tuberculosis (TB). Three of six patients were Yemenite Jews, an ethnic group constituting only 10.8% of the dialysis population; thus, Yemenite Jews appear to be especially at risk among Israeli dialysis patients. Fever of unknown origin was the most frequent presenting symptom. In four patients, previous TB of the lungs was documented. These data support the view of reactivation of dormant TB as the main pathogenetic pathway for the development of the active disease. Two patients died, whereas four recovered on triple therapy with isoniazid, rifampicin and ethambutol.

PTH was shown to stimulate RNA and heme synthesis in 12-13 days embryonic mouse liver erythroid cells, thus expressing an erythropoietin-like effect. Incubation of erythroid precursors with 1,25(OH)2D3 had no effect on heme synthesis, and increased the RNA synthesis only slightly, thus showing no enhancement effect of 1,25(OH)2D3 on the PTH stimulating effect on erythropoiesis.

The platelet element content was determined by semiquantitative X-ray microanalysis in 6 patients with chronic renal failure. The patients showed a different degree of thrombocytopathy expressed by impaired adhesiveness, epinephrine-induced aggregation and platelet factor 3 availability. The microanalysis indicated significantly increased quantities of phosphorus and copper in patients' platelets. Sodium and zinc showed a decrease in about half of the patients, whereas iron was significantly increased in at least 50% of the patients. Magnesium and potassium did not show any difference from the control. The results of sulfur, chlorine and calcium did not reveal a consistent pattern.

A patient with medullary cystic disease presented with a combined tubular dysfunction, including severe salt wasting, renal tubular acidosis types I and IV, and marked aldosterone resistance. High-dose mineralocorticoid treatment partially corrected the defect in potassium excretion and did not affect natriuresis. Plasma aldosterone level was more than 30 times the upper normal level and was decreased but not normalized by captopril administration and volume expansion. The severe hemodynamic and metabolic consequences of these defects were corrected by renal transplantation.

During the period 1975-81, autopsies were performed in 15 patients who had been treated by long-term hemodialysis and who had no clinical or family history of polycystic disease. Ten of the patients were found to have bilateral cystic disease of the kidneys. In 3 of the 10 patients with cystic kidneys, tumors were found: a solid tubular adenoma in one, multiple bilateral papillary adenomas in another, and clear cell tubular carcinoma in the third. Hemorrhages were not detected in any of the patients. The results of our study confirmed that patients on hemodialysis have a very high incidence of acquired cystic disease and are at high risk of developing neoplasms in their contracted kidneys.

A patient with a false aneurysm of the iliac artery following removal of a right allograft developed a prolonged fever and anemia of unknown origin. The patient's condition was initially misinterpreted largely because these symptoms were attributed to dialysis treatment. This case emphasizes fever and anemia as the sole manifestations of a false aneurysm appearing as a late complication of kidney transplantation.

A patient on hemodialysis treatment developed hepatocellular carcinoma (HCC) after long-term therapy with androgenic anabolic steroids. The tumor progressed very rapidly, and there was no evidence of regression despite discontinuation of the drug. In view of the evidence of an increased of malignancy in patients with chronic uremia and hemodialysis, and of the higher frequency of HCC correlated to treatment with C17-alkylated anabolic steroids, it is necessary to further evaluate the efficiency of this treatment in the aforementioned group of patients.

Hyperprolactinemia is known to cause impotence in patients with normal renal function and elevated serum prolactin levels (SPLs) have also been reported in uremia. This study was undertaken to examine a possible role of elevated SPLs in the impotence of male patients undergoing chronic hemodialysis (CHD). SPLs in 16 male patients undergoing CHD were evaluated using a homologous double-antibody radioimmunoassay with prolactin isohormones isolated from human amniotic fluid. Patients were divided in 2 groups: 6 patients were sexually impotent and 10 sexually potent. Patients with emotional disturbances or marital conflicts known to cause impotence were excluded from the study. The SPLs of the impotent patients were found to be significantly elevated in comparison to the levels of the potent patients (136.7 +/- 28.2 vs. 37.3 +/- 2.7 ng/ml, p less than 0.001). Furthermore, in 2 patients who were successfully treated with bromocriptine to suppress hyperprolactinemia, recovery of sexual potency was noted. Thus, sexual impotence in male CHD patients seems to be associated with marked hyperprolactinemia. It is suggested that elevated SPLs may be an important cause of impotence among CHD patients.

A patient with end-stage renal disease due to nephronophthisis developed nephrotic syndrome following renal transplantation. Renal biopsy revealed rejection glomerulopathy with massive linear deposition of immunoglobulin (Ig) G and complement C3 along the glomerular and tubular basement membranes. The association of nephrotic syndrome with linear deposition of Ig is rare in chronic rejection of kidney allografts. The nephrotic syndrome in this case responded to treatment with plasmapheresis.