Search

We report two cases of acute renal failure in patients with arteriosclerosis obliterans treated by intravenous infusion of naftidrofuryl oxalate. At renal biopsy the histological lesions were identical with those found in ARF due to hyperoxaluria of other causes, revealing tubular epithelial necrosis and massive intra-tubular precipitation of calcium oxalate monohydrate (Cl) crystals. A second study was then conducted in four other patients with arteriosclerosis obliterans to evaluate serum and urinary levels of oxalate, and crystalluria during the intravenous administration of 800 mg of naftidrofuryl oxalate per day for 10 days. During the course of treatment, the serum and urinary oxalate levels were found to increase substantially, with the gradual onset of massive Cl crystalluria. These results indicate that naftidrofuryl oxalate was responsible for the acute renal failure in the first two patients. High intravenous doses of naftidrofuryl oxalate must be used cautiously, with close surveillance of renal function. [ABSTRACT FROM PUBLISHER]

As arachidonic acid metabolites are implicated in hypersensitivity reactions, we measured arachidonic acid metabolites of dialysed patient's granulocytes, preincubated with different dialysis membranes. Results indicate that cuprophan and cellulose acetate membranes partially inhibit in vitro production of 15-HETE and 5-HETE, whereas polyacrylonitrile membrane does not. This suggests that polyacrylonitrile is a more biocompatible membrane. [ABSTRACT FROM PUBLISHER]

A 25-year-old woman who was 20 weeks pregnant developed systemic lupus erythematosus with acquired ichthyosis and pyoderma gangrenosum. The course of these dermatoses suggests that an immunopathological mechanism was implicated in their pathogenesis. [ABSTRACT FROM AUTHOR]

Focuses on acute renal failure and hematuria in marathon runners, examining the role of glomerular bleeding in tublar injury in the risk of renal failure in runners and referencing the case report of a 46-year-old male marathon runner. Details on the symptoms the runner presented; Factors which contributed to the onset of renal failure; Information on the tests conducted on the patient; Treatment administered to the patient.

Background: Macrophage-colony stimulating factor (M-CSF) is the principal factor for survival of monocytes and macrophages that play an important role in allograft rejection. We studied M-CSF serum levels during successful renal transplantation and acute graft rejection., Methods: A total of 114 kidney allograft recipients were assessed for M-CSF levels by enzyme-linked immunosorbent assay (ELISA)., Results: M-CSF serum levels were elevated in pre-transplant haemodialysis patients (611+/-355 IU/ml vs 168+/-61 in normal controls, P<0.01). Following successful renal transplantation, M-CSF decreased in the first month, stabilizing at 257+/-222 IU/ml (not significantly different from normal controls) in 52 post-transplant stable patients. There was no correlation between M-CSF level and creatinine clearance. M-CSF levels increased significantly (2-5 times) during biopsy-proven acute rejection episodes in 20 of 25 patients. All rejection episodes were successfully treated and serum M-CSF decreased rapidly to pre-rejection levels in 17/20 patients. In contrast, in five patients with cyclosporin toxicity and four patients with other causes of allograft dysfunction, M-CSF serum levels did not change., Conclusions: M-CSF serum level might be a specific marker of acute rejection. The source of increased production during rejection warrants further investigation, with infiltrating T cells and resident kidney cells being likely candidates.

Background: The indwelling venous catheter such as Dual-Cath or Twin-Cath is widely used in haemodialysis. Although the manufacturer recommends filling the catheter lumen with heparin after the dialysis session to prevent clotting, little is known about the systemic effects of such a procedure., Methods: Twenty haemodialysis patients with Dual-Cath were studied. Dialysis anticoagulation was achieved by injecting a bolus of dalteparin. The patient/control ratio of activated partial thromboplastin time (aPTT) was determined at the end of the session immediately before and 10 min after locking with 2 ml of undiluted heparin (10,000 U/catheter). We also determined the catheter volume for each patient and measured aPTT immediately before and 10 min after heparin locking with this patient-specific volume. Catheter patency was followed over a 2-week period., Results: The aPTT values determined at the end of two consecutive dialysis sessions were nearly normal, respectively 1.29 (+/-0.17) and 1.33 (+/-0.22), whereas all patients had uncoagulable blood (aPTT >3.75) 10 min after locking with 2 ml of heparin. When catheter volumes were individually calculated, they were found to be substantially lower than 2.0 ml (1.21+/-0.12 for the arterial branch and 1.27+/-0.13 for the venous branch). aPTT was only 2.42+/-0.73 10 min after locking with the estimated volumes except in one patient (aPTT >3.75). No catheter clotting was observed despite these smaller locking volumes., Conclusions: A risk of inducing serious bleeding does indeed exist with Dual-Cath heparin locking, especially in postoperative patients. This risk can be reduced by measuring catheter length at the time of placement in order to ensure an appropriate lock volume. Sodium citrate, polygeline, or urokinase are possible alternatives to heparin.

N-acetyl-seryl-aspartyl-lysyl-proline (AcSDKP) is a physiological inhibitor of hematopoiesis that is maintained at stable levels in normal plasma. Its degradation in vivo and in vitro by angiotensin-converting enzyme (ACE) accounts for the high plasma concentrations of AcSDKP in patients treated with ACE inhibitors. Because ACE inhibitors can induce anemia in some patients, we measured plasma AcSDKP concentrations in 176 patients with chronic renal failure: 120 hemodialysis (HD) and 56 nondialysis (nD) patients, 39 of whom were administered ACE inhibitors. We studied the relationships between AcSDKP levels, hematologic parameters, and recombinant human erythropoietin (rHuEPO) requirements in these patients. AcSDKP levels were significantly greater in HD (10.3 +/- 3.9 pmol/mL) and nD (3.1 +/- 1.8 pmol/mL) patients not administered ACE inhibitors than controls (1.8 +/- 0.2 pmol/mL). In all patients, treatment with ACE inhibitors significantly increased these levels fourfold. HD sessions significantly decreased AcSDKP concentrations by 66% and reduced the predialysis in vitro half-life of AcSDKP (270 +/- 109 minutes) to values (182 +/- 67 minutes) not significantly different from those of controls or nD patients. Most HD patients treated with ACE inhibitors had AcSDKP levels greater than 24 pmol/mL (the greatest concentration found in other nD and HD patients). Only in this group of patients did weekly doses of rHuEPO correlate with AcSDKP levels. Our results show that renal function is essential to maintain stable AcSDKP plasma levels, and at high levels, AcSDKP acts as a uremic toxin causing partial resistance to erythropoietin and inhibiting erythropoiesis.

Background: The theoretical aim of maintenance cyclosporine monotherapy (mCsA) after kidney transplantation is to reduce the incidence of the metabolic complications of corticosteroids and to minimize the adverse effects of excessive long-term immunosuppression. This study was performed in low-immunological-risk cadaveric kidney transplant recipients to evaluate the risks and benefits of mCsA and the long-term graft survival, and to determine the factors predicting success of this policy., Methods: The multicenter retrospective study was conducted in 329 Caucasian patients receiving mCsA out of 728 first cadaveric kidney transplant recipients. The inclusion criteria were: HLA antibodies < or =25%, serum creatinine <200 micromol/L, and no rejection or only one rejection episode. At the end of the study, we compared the group of patients successfully treated with mCsA (successful group) with those requiring additional immunosuppressive agents (unsuccessful mCsA group)., Results: Overall patient and graft survival rates for the 728 first cadaveric graft were 92% and 64%, respectively, at 8 years. Out of 329 patients enrolled in mCsA, 240 were maintained on this treatment and 89 were withdrawn (3 deaths, 18 graft losses, 68 functional grafts). The 8-year graft survival in the 329 enrolled mCsA patients was 84%, 95% in the successful mCsA group, and 70% in the unsuccessful mCsA group. Multivariate analysis showed that the factors predicting success of mCsA were: donor age <40 years (P = 0.001), serum creatinine at mCsA initiation <125 micromol/L (P = 0.02), no rejection episode before mCsA initiation (P = 0.005), and glomerulopathy as the primary renal disease (P = 0.001)., Conclusion: Numerous kidney transplant recipients with a low immunological risk and good and stable renal function may benefit from discontinuation of prednisone and azathioprine in order to reduce the complications related to these drugs. This therapeutic approach had no adverse impact on the overall long-term graft survival for "low risk" and successful patients.

Background: The production of monocytic cytokines by isolated mononuclear cells after stimulation by phytohaemagglutinin (PHA) and lipopolysaccharide (LPS) is generally increased in haemodialysed (HD) patients. We performed whole blood (WB) cultures to evaluate cytokine production by blood cells inside their complex cellular and humoral network., Methods: Diluted whole blood from HD patients (collected before dialysis) and controls was cultured alone with PHA (2.5 microg/ml) or LPS (1 and 3 microg/ml). Supernatants were collected after 24 and 48 h of culture, and concentrations of IL-1 beta, IL-6, TNF-alpha, sIL-6R and IL-1Ra were determined by ELISA., Results: The low spontaneous production of IL-1beta, IL-6 and TNF-alpha in both patients and controls was not significantly modified by PHA. The lower dose of LPS (1 microg/ml) induced a significant but lower increase in production of IL-1beta, IL-6 and TNF-alpha in patients than in controls. In contrast, while it did not further increase their production in controls, the higher concentration of LPS (3 microg/ml) still increased their production in patients to the same level than in controls. The plasma concentrations of sIL-6R were higher in patients than in controls. In both groups, the sIL-6R concentration did not vary during the culture period whether the cells were stimulated or not with LPS or PHA. This suggests that the increased plasma levels of sIL-6R were not produced by blood cells. Despite a similar significant LPS and PHA induced production of IL-1Ra, the IL-1Ra/IL-1beta ratio was always higher in patients than in controls., Conclusion: Monocytes from HD patients in WB cultures are hyporesponsive to PHA and LPS for their IL-1beta, TNFalpha and IL-6 production in contrast to isolated monocytes that demonstrate signs of activation. If it reflects the in vivo situation it could partly explain the immune defect in uraemic and haemodialysed patients. Higher sIL-6R/IL-6 and IL-1Ra/IL-1beta ratios could also participate to the complex immune disturbances of HD patients by reducing the biological activity of two cytokines playing a major role in the immune and inflammatory network.

Paraoxonase is an esterase that hydrolyzes organophosphate compounds. The enzyme is associated with HDL and could protect LDL against peroxidation, which suggests a possible involvement of paraoxonase in the antiatherogenic properties of HDL. Paraoxonase activity has been shown to be low in patients with myocardial infarction, diabetes mellitus, or familial hypercholesterolemia. Because cardiovascular disease is the main cause of death in chronic renal failure, serum paraoxonase activity was measured by spectrophotometry using three synthetic substrates (phenyl acetate, paraoxon, and 4-nitrophenyl acetate) in 305 patients with kidney disease, including 47 patients with non-end-stage chronic renal failure, 104 patients treated with hemodialysis, 22 patients treated with peritoneal dialysis, and 132 renal transplant patients. Patients were compared with two groups of aged-matched control subjects (total number = 195). Especially with 4-nitrophenyl acetate, paraoxonase activity was lower in patients with some degree of renal insufficiency (chronic renal failure [P < 0.05], chronic hemodialysis [P < 10(-4)], chronic peritoneal dialysis [P < 10(-4)]) than in control subjects. In transplant patients, paraoxonase activity was not found to be different from that in control subjects. The decrease of paraoxonase activity and thus the reduction of its antiatherogenic properties in renal failure could be an essential factor of premature vascular aging, especially when dialysis is used. Renal transplantation seems to restore paraoxonase activity.

The immunodeficiency of patients with chronic renal failure (CRF) is related to multiple and complex alterations of the cytokine network and of its target cells such as T or B lymphocytes, monocytes, fibroblasts or endothelial cells. Chronic activation of monocytic functions is recognized as a key factor in these immunological disorders. Since macrophage colony stimulating factor (M-CSF) is essential for the activation of several functions of monocytes and macrophages and their production of cytokines such as interleukin-1, interleukin-6, and tumor necrosis factor alpha, we investigated its involvement in patients with CRF. When measured by ELISA, M-CSF serum levels were significantly higher in patients with progressive CRF and those on hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD) than in controls. M-CSF serum levels did not correlate with the degree of renal insufficiency and were probably related to complex alterations in its production and/or degradation by the specific M-CSF receptors of macrophages. In HD patients the M-CSF serum concentrations inversely correlated with the number of circulating lymphocytes and were significantly higher in anemic patients requiring treatment with erythropoietin. Our results suggest that M-CSF may play a role in altering the immune system in uremic patients by maintaining in the circulation and tissues permanently primed monocytes and/or macrophages that can then be triggered to an activated state by secondary stimuli such as endotoxins, complement components, other cytokines or contact with foreign surfaces.

Renal manifestations of the "primary" antiphospholipid syndrome are rare. We report the case of an athletic 35-year-old man with an unremarkable medical history who suddenly developed hypertension and a renal infarction. Laboratory and radiological investigations showed a complete thrombosis of the infrarenal aorta, extensive collateral circulation arising from the superior mesenteric artery, and the primary antiphospholipid syndrome. Eight cases of renal infarction have previously been reported in the primary antiphospholipid syndrome. To our knowledge, this represents the first case of an infrarenal aortic thrombosis attributable to this syndrome.

Crystalluria is important in the evaluation of patients with urinary stone and is more frequently encountered in elderly than in younger adults. After noting that calcium oxalate monohydrate crystalluria was higher in elderly patients, we undertook a study to determine if oral treatment with naftidrofuryl oxalate, a drug frequently prescribed for elderly patients in France, was associated with crystalluria. The presence of early morning crystalluria was assessed in non-stone-forming patients hospitalized in a geriatric department. We studied 251 patients without a history of nephrolithiasis (mean age; 81.6 +/- 8.5 years) of whom 49 had been treated orally with naftidrofuryl oxalate at a mean dosage of 485 +/- 120 mg/24h. We identified and quantified the crystals in one early morning urine sample kept at room temperature. The frequency of crystalluria in elderly patients without stones who were not taking naftidrofuryl oxalate was 31.7% compared with only 6% in the general adult population. In this group, mainly calcium phosphate crystals were found. In patients who received naftidrofuryl oxalate, the frequency of crystalluria was 51% of which the major component was calcium oxalate monohydrate and not calcium phosphate. Naftidrofuryl oxalate may enhance crystal formation in elderly patients. This should be taken into account, particularly when other predisposing factors for nephrolithiasis are present, and a preventive increase in fluid intake considered.

1. There is no experimental proof that renal insufficiency is a necessary condition for hypertension during erythropoietin treatment. 2. The present study compares the effect of 3 weeks treatment with r-hu EPO (50 i.u./kg) on systolic blood pressure (SBP), haematocrit and plasma cGMP in an animal model of chronic renal failure (remnant kidney model excision) and sham-operated rats. 3. Sub-total nephrectomy induced a significant fall in haematocrit and a significant increase in plasma creatinine levels. Treatment with r-hu EPO resulted in a significant haematocrit increase in uraemic as well as in non-uraemic rats. Despite this effect, r-hu EPO treatment had no effect on SBP in sham-operated rats. On the contrary, this treatment caused significant SBP elevation in uraemic rats; in these rats, SBP increase did not correlate with haematocrit increase. 4. Plasma cGMP concentrations were significantly higher in uraemic compared to sham-operated rats and were not modified by r-hu EPO treatment. 5. This study provides evidence that renal insufficiency in rats is a prerequisite for the development of hypertension during erythropoietin treatment.

Bladder lithiasis is a frequent complication in paraplegics and tetraplegics. We report on a patient where treatment of a urinary infection with antibacterial sulfamides was the causative factor in the formation of bladder stones.

We report a case of hypokalemic flaccid quadriplegia with sudden respiratory arrest in a 38-year-old woman discovered to have distal renal tubular acidosis which lead to the diagnosis of primary Sjögren's syndrome. This case is compared to 8 similar cases previously described in the literature.

Serum theophylline and metabolites (methyluric acids, mono- and dimethyl xanthines) concentrations from uremic patients, either with end-stage renal failure or on peritoneal dialysis or maintenance hemodialysis, were investigated by HPLC and compared with those obtained in non-uremic subjects. We conclude that in uremic patients serum theophylline metabolites, particularly serum 1,3-dimethyluric acid, are significantly higher than in non-uremic subjects even when serum theophylline is lower. A slight increase in the free fractions of serum theophylline was also observed in these patients. All these findings could explain the toxicity signs noted in some patients with chronic renal failure and treated with very low doses of theophylline.

The proteinuria of fifteen patients treated with just aminoglycoside or aminoglycoside and either penicillin or cephalosporin was studied. The proteinuria was analysed by means of immunoelectrophoresis, acetate cellulose electrophoresis, thin-layer polyacrylamide gel electrophoresis and sodium dodecylsulphate acrylamide gel electrophoresis. We observed a urinary excretion of free immunoglobulin light chains and an increased urinary excretion of lysozyme in all cases. The increase in urinary excretion of beta-2-microglobulin and retinol-binding-protein appeared only in patients treated with aminoglycoside and cephalosporin. These disturbances disappeared a few days after the treatment was discontinued.

Studies of the serological development after 26 renal transplants confirm the high frequency of antibody rises not only against the herpes virus group, but also against other virus groups such as measles, Coxsackie B viruses. These antibody rises correlate with febrile episodes and hepatic dysfunction in which CMV is the most often involved. However, the frequency of antibody rises against various viral antigens without any clinical event to suggest viral etiology; the lack of concomitant virus isolation (except the herpes group), as well as the ocurrence of simultaneous antibody rises against several viruses, all suggest that some of these various antibody rises observed may be related to immunological dysfunction rather than to virus infection.

Various analytical methods are available to help identify the presence of drugs in urinary calculi. Using infrared spectrophotometric analysis, nonmetabolized flumequine was identified in a protein calculus from a patient who had taken the drug for a urinary tract infection. Free flumequine can precipitate in an acidic environment.

Two patients are reported in whom early and irreversible renal allograft rejection was associated with passage of necrotic papillary material in the urine. Evidence is presented for a causal relationship between rejection and medullary necrosis. Passage of a papilla is regarded as a definite indication for graft exploration.

Contrast nephropathy is a recognized complication of arteriographic procedures; usually, it consists of a mild deterioration of renal function. In an attempt to understand better the mechanisms involved, we conducted a prospective study before and after arteriography that monitored the urinary elimination of high- and low-molecular weight proteins, the urinary activity of tubular enzymes, and renal clearances of 27 patients. We detected a noticeable and transient nonselective proteinuria of glomerular origin together with moderate signs of tubular damage and a stable renal function. We did not identify any risk factor. Contrast media may alter the disposition of charges along the glomerular filtering membrane in a way that promotes proteinuria; consequently, the massive flow of proteins may injure the tubular cells.