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Biomedical subjects

U Helmchen

Publications and source records attributed to U Helmchen.

At least 19 recordsLinked to original sources
PubMed1992

[Interstitial lupus nephritis].

A 17-year old-male presented with a 6-week history of weight loss, lassitude and calf pains. On examination he was very pale. Laboratory tests showed a very high erythrocyte sedimentation rate (155 mm in the first hour), anaemia (haemoglobin 10.1 g/dl), and a raised serum creatinine of 1.54 mg/dl. Microhaematuria (5-10 erythrocytes/microliter) and pronounced pyuria (500 leucocytes/microliter) were present, but the urine was sterile and there was no increase in albumin excretion. The serum IgG was raised to 75.7 g/l, suggesting an autoimmune disorder. Anti-nuclear antibodies (titre 1 : 1920) and anti-double-stranded DNA antibodies (31 U/ml) were present, while the serum complement C4 was decreased to 0.11 g/l. Renal histology showed an interstitial nephritis without glomerular involvement, while the bone marrow showed vasculitis accompanied by a prominent plasma-cell infiltrate. A diagnosis of interstitial nephritis associated with systemic lupus erythematosus was made, with asymptomatic cardiac and hepatic involvement. Renal function recovered rapidly with prednisolone therapy (initial dose 2 mg/kg.d). While glomerulonephritis is the most common lupus-associated renal disorder, isolated interstitial nephritis may occur in some cases, often with an absence of proteinuria.

Adolescent↗
PubMed1992

Tubular function and histological findings in ifosfamide-induced renal Fanconi syndrome--a report of two cases.

Two patients developed renal Fanconi syndrome (RFS) after intensive long-term chemotherapy for metastatic Ewing sarcoma and disseminated neuroblastoma. Whereas RFS was diagnosed in patient 1 before he developed osteomalacia, patient 2 experienced severe rickets and growth retardation. Renal function studies revealed slight glomerular impairment and severe tubular defects leading to increased excretion of glucose, amino acids, inorganic phosphate and low molecular weight proteins, indicating proximal tubular damage. Patient 2 additionally showed distal tubular dysfunction with acidosis and diminished concentrating capacity. Renal biopsy in patient 1 revealed marked proximal tubular defects without interstitial lymphocytic infiltration. In both patients renal damage could most likely be ascribed to previous ifosfamide (IFOS) therapy. Our patients showed no improvement in renal function after cessation of IFOS treatment, indicating a poor prognosis of once established RFS after IFOS therapy. Measurement of tubular reabsorption capacities provides exact information on the extent of tubular toxicity induced by IFOS and may be used to monitor IFOS treated patients.

Adolescent↗
PubMed1992

Adverse effect of the calcium channel blocker nitrendipine on nephrosclerosis in rats with renovascular hypertension.

The effect of a 6-week treatment with the calcium channel blocker nitrendipine or the angiotensin converting enzyme inhibitor enalapril on blood pressure, albuminuria, renal hemodynamics, and morphology of the nonclipped kidney was studied in rats with two-kidney, one clip renovascular hypertension. Six weeks after clipping of one renal artery, hypertensive rats (178 +/- 4 mm Hg) were randomly assigned to three groups: untreated hypertensive controls (n = 8), enalapril-treated (n = 8), or nitrendipine-treated (n = 10). Sham-operated rats served as normotensive controls (128 +/- 3 mm Hg, n = 8). After 6 weeks of treatment, renal hemodynamics (glomerular filtration rate and renal plasma flow) were measured in the anesthetized rats. Renal tissue was obtained for determination of glomerular size and sclerosis. Enalapril but not nitrendipine reduced blood pressure significantly. After 6 weeks of therapy, glomerular filtration rate was not different among the studied groups. Renal plasma flow increased, but albumin excretion and glomerulosclerosis did not change after enalapril treatment. In contrast, in the nitrendipine-treated group albuminuria increased from 12.8 +/- 2 progressively to 163 +/- 55 compared with 19.2 +/- 9 mg/24 hr in the hypertensive controls. Furthermore, glomerulosclerosis index was significantly increased in the nitrendipine-treated group compared with the hypertensive controls (0.38 +/- 0.1 versus 0.13 +/- 0.04). In addition, glomerular size was higher in the nitrendipine-treated group (14.9 +/- 0.17 10(-3) mm2) but lower in the enalapril-treated group (11.5 +/- 0.15 10(-3) mm2) compared with the hypertensive controls (12.1 +/- 0.17 10(-3) mm2).(ABSTRACT TRUNCATED AT 250 WORDS)

Albuminuria↗
PubMed1992

Morphologic and functional consequences of immune-mediated mesangiolysis: development of chronic glomerular sclerosis.

The i.v. injection of a rabbit anti-rat thymocyte serum (ATS) induces mesangiolysis in rats, followed by a mesangioproliferative glomerulonephritis (4 to 7 days after antibody). This proliferative lesion disappears 4 to 6 wks after antibody. In order to induce an antibody-mediated sclerotic glomerular disease, uninephrectomized rats received ATS twice at 6-wk interval. At 6 months after the first antibody injection, albuminuria, arterial blood pressure, and inulin clearances were evaluated and renal morphologic studies were performed. At the time of evaluation, mean arterial blood pressure and inulin clearances were not different between animals that received the antibody and uninephrectomized controls. Rats that were injected with antibody, however, had significantly higher albuminuria compared with that of controls. Glomeruli of rats with ATS revealed expansion of the glomerular mesangial matrix and focal sclerosis. A semiquantitative morphologic analysis revealed an increased incidence of glomerular lesions and a higher glomerular damage index in kidneys of nephritic rats. These data demonstrate that the repetitive injection of ATS to unilaterally nephrectomized rats induces a model of chronic glomerular sclerosis.

Albuminuria↗
PubMed1992

A rat model of progressive chronic glomerular sclerosis: the role of thromboxane inhibition.

In order to evaluate a possible role of thromboxane A2 (TxA2) in the pathophysiology of chronic glomerular disease, we studied the effect of a 12-wk combined treatment with the thromboxane receptor blocker Daltroban (D) and the thromboxane synthesis inhibitor UK 38485 (UK) on glomerular function and morphology in a rat model of chronic progressive glomerular injury. The glomerular lesion was induced in unilaterally nephrectomized rats by the repeated i.v. injection of an antibody directed against mesangial cells. Control rats were uninephrectomized. Three months after the first antibody injection before D and UK treatment, albuminuria (35.8 +/- 3.6 mg/24 h) and glomerular TxB2 formation (146 +/- 20 pg/mg of protein/min) were significantly higher compared with control values (albuminuria, 14.3 +/- 3.5 mg/24 h; TxB2, 59 +/- 16 pg/mg/min). Six months after antibody, albuminuria in nephritic rats had increased to 135 +/- 17 mg/24 h. In nephritic rats treated with D plus UK, albuminuria (44 +/- 12 mg/24 h), however, was significantly (P less than 0.001) inhibited. Quantitative morphological analysis (glomerular damage index) 6 months after antibody revealed significantly (P less than 0.001) increased glomerular lesions in nephritic rats (0.353 +/- 0.095) compared with that in uninephrectomized controls (0.045 +/- 0.014). The treatment of rats with D and UK significantly (P less than 0.001) reduced the glomerular damage index (0.101 +/- 0.004) in nephritic rats. D plus UK treatment reduced glomerular TxB2 formation but increased prostaglandin E2 and 6-keto prostaglandin F1 alpha release by isolated glomeruli. This study demonstrates that interventional treatment with D and UK ameliorates albuminuria and glomerular morphological lesions in a rat model of immunologically induced progressive glomerular injury.

Albuminuria↗
PubMed1992

Cytomegalovirus detection in kidney transplants: results obtained from the polymerase chain reaction.

Kidneys from twelve renal transplant recipients were examined prior to and after graft failure and explantation. The investigations included conventional light and electron microscopy and the analysis of human cytomegalovirus-related viral proteins and viral DNA. Nucleic acid hybridization studies were conducted on kidney explants by an in situ method using DNA probes and by the polymerase chain reaction employing primers and probe for immediate early gene targets. In none of the cases did light and electron microscopy including immunohistochemistry for human cytomegalovirus reveal active infection in punch biopsies or explants. Interestingly, in situ hybridization also failed to detect human cytomegalovirus even in two cases with seroconversion, while the polymerase chain reaction was positive. The polymerase chain reaction disclosed only two additional positive cases within the residual group of explanted kidneys. In our hands, the polymerase chain reaction was the only potent direct detection method for cytomegalovirus in transplanted human kidneys.

Adult↗
PubMed1992

Kidney transplantation in Alport's syndrome: long-term outcome and allograft anti-GBM nephritis.

Anti-glomerular basement membrane (anti-GBM) nephritis occurring in kidneys transplanted in patients with Alport's syndrome (AS) has been reported repeatedly. Therefore, we studied graft survival and course of renal function in all 30 AS patients grafted at Hannover Medical School and compared them with non-diabetic, age and sex matched patients, transplanted on the date closest to the transplantation of the AS patient. Serum creatinine, proteinuria, urinary sediment and anti-GBM antibodies were examined in all AS patients with functioning grafts. Cases of patient or graft loss in the AS group were analyzed retrospectively. One- and five-year patient survival was 100 and 91% in AS and 89 and 78% in controls (p > 0.05, respectively). One- and five-year first graft survival was 79 and 66% in both groups. Graft histology was available in 34 biopsies obtained from 21 kidneys in 15 AS patients. Anti-GBM nephritis was not detected in any of the biopsies. No graft was lost due to anti-GBM nephritis. Anti-GBM antibodies were detectable temporarily only in one AS patient. He also had linear IgG staining in his graft GBM, but no other signs of anti-GBM nephritis. We conclude that patient survival and graft survival in AS patients following kidney transplantation is not different from non-AS patients. Allograft anti-GBM nephritis is a rare complication in patients with Alport's syndrome.

Adult↗
PubMed1991

[Anti-basal membrane glomerulonephritis after homologous kidney transplantation in hereditary Alport's nephropathy].

A patient, born in 1968, was found at the age of 9 years to have Alport's syndrome. In his 20th year, when in terminal renal failure, his father's kidney was transplanted into him. 14 months later there was a sudden worsening of his renal function after a varicella infection; for the first time antibodies against the glomerular basal membrane (GBM) were detected. Despite an increase in prednisolone dosage and 6 plasmaphereses chronic haemodialysis again became necessary. Renal biopsy revealed necrotizing intra- and extracapillary glomerulonephritis. Simultaneously there was a raised anti-NC-1-antibody titre (1:80) in the serum. After removal of the transplant the titre fell to normal. The NC-1 antigen, a component of the GBM in healthy persons, may be absent in Alport's syndrome. An analysis of the few cases of anti-GBM glomerulonephritis in renal transplants of patients with Alport's syndrome may make it possible to recognize factors which precipitate or favour this form of glomerulonephritis.

Adult↗
PubMed1991

Kidney biopsy findings in cyclosporine-treated patients with insulin-dependent diabetes mellitus.

Renal biopsy specimens of 40 patients with recent-onset insulin-dependent diabetes mellitus treated with cyclosporine (CSA) for 6-29 months were examined. Cyclosporine-associated chronic vascular interstitial toxicity of moderate intensity was found in 10 patients (25%). The most prominent lesions were interstitial fibrosis and tubular atrophy. Arteriolopathy was less pronounced and glomerular damage unremarkable. A significant correlation exists between the extent of tubular atrophy and CSA trough whole blood levels. These data indicate that the development of CSA-associated chronic nephropathy is dose-dependent.

Adolescent↗
PubMed1991

Candidiasis visualised by proteinase-directed immunofluorescence.

The secretory aspartic proteinases of Candida albicans and C. tropicalis are potential factors for virulence produced during infection. By indirect immunofluorescence, we have demonstrated proteinase antigen on elements of both species in deparaffinized tissue sections derived from clinical cases of mucosal and deep-seated candidiasis. Occasionally, we observed a halo of fluorescence in the close vicinity of candidal cells, which may reflect secretion of the enzyme. In kidneys, a ring of amorphous fluorescent material surrounding candidal colonies may illustrate alkaline denaturation of secreted enzyme within a pH gradient, which is generated by the fungus. Our findings support the view that candidal proteinase may be a diagnostically relevant antigen.

Adult↗
PubMed1990

A new method for conservative renal surgery--experimental and first clinical results.

So far two methods for prolonging the tolerance of renal ischemia are available: 1) surface cooling with crushed ice and 2) perfusion cooling with an extracellular-like solution. Both methods use only the principle of reducing metabolism through cooling. While rewarming during surgery the ischemic protection is lost, or the kidney must be cooled once again. Therefore, a new preservation solution should reduce energy consumption due to its composition in addition to cooling. For open heart surgery, the HTK solution by Bretschneider is already used clinically. In 71 dog kidney experiments, the ischemic time kidneys could tolerate was prolonged by this solution from 15 to 120 min at 35 degrees C and from 45 to 360 min at 25 degrees C. After 2 h of ischemia at 30 degrees C glomerular filtration rate was about 20 ml/min.100gww within 3 h of reperfusion. After six postoperative days the filtration rate was 40 ml/min.100 gww. No ischemic damage could be recognized by histological investigations. The clinical effectiveness of this method was shown in 7 clinical applications. Ischemic duration lasted up to 113 min, and blood creatinine was between 0.8 and 2.4 mg% at the 6th postoperative day. Use of this preservation technique thus leads to improved kidney function immediately following operation. Longer ischemia can be tolerated by a kidney thus protected, and using this technique excellent visibility can be achieved during intrarenal surgery, simplifying, for example, tumor extirpation.

Animals↗
PubMed1990

Association of spondylo-epiphyseal dysplasia with nephrotic syndrome.

The association of a spondylo-epiphyseal dysplasia and growth failure with the nephrotic syndrome was found in three boys. Renal biopsy performed on two revealed focal and segmental glomerulosclerosis. The nephrotic syndrome occurred at the age of 3-7 years, leading to end-stage renal failure in all patients. Growth failure persisted after successful renal transplantation. This association may represent a distinct disease entity.

Child↗
PubMed1990

[Recurrent post-infectious immune complex glomerulonephritis with persistent activation of the alternative complement pathway].

Recurring upper respiratory tract infections in a previously healthy 4 years old boy led to an acute nephritic syndrome requiring haemodialysis. Renal biopsy showed poststreptococcal like immune complex glomerulonephritis with subepithelial humps, C3 deposition and crescent formation. Renal function improved after methyl-prednisolone pulse therapy. Two relapses occurred in the following six months which responded to immunosuppressive therapy. 21 months following the first presentation the boy has normal glomerular filtration rate but persistent glomerular proteinuria and haematuria. Detailed complement analyses revealed a persistent activation of the alternate pathway.

Child, Preschool↗
PubMed1989

[Relapsing polychondritis].

For three months a 17-year-old boy had been suffering from laryngitis, pharyngitis and conjunctivitis, weight loss, nocturnal sweating and signs of changing cranial-nerve involvement (dizziness, nausea, nystagmus). The diagnosis of recurrent polychondritis was made only when, in addition to a definite inspiratory stridor there also developed a painful swelling of the left ear cartilage and a saddle nose due to loss of the cartilaginous portion of the nasal skeleton. Histological examination of the inflamed ear cartilage confirmed the diagnosis. After treatment with prednisone (100 mg daily, gradually reduced to 25 mg) and azathioprine (100 mg daily, increased to 150 mg after three weeks), there was clinical improvement, but the airway resistance (R = 6.2 cm H2O.s/l) rose further, requiring tracheostoma twelve months after onset of symptoms.

Adolescent↗
PubMed1989

Effect of thromboxane synthesis inhibition in a model of membranous nephropathy.

The effect of the thromboxane synthesis inhibitor UK 38485 on glomerular filtration rate (GFR) and proteinuria was evaluated in a rat model of unilateral membranous nephropathy. Two and 24 hours following perfusion of kidneys with cationized human IgG and i.v. administration of anti-human IgG-antiserum (in situ ICGN), glomerular thromboxane B2 (TxB2) formation was significantly higher (2 hr: 448 +/- 116 pg/mg protein/min; 24 hr: 173 +/- 21 pg/mg protein/min) compared to control (C) kidneys (2 hr: 173 +/- 21 pg/mg protein/min, P less than 0.005; 24 hr: 154 +/- 17 pg/mg protein/min, P less than 0.025). Two and seven days after induction of ICGN these differences were no longer present. Pretreatment with the thromboxane synthesis inhibitor UK 38485 prevented the decrease in GFR, which occurred two hours after induction of the glomerular disease (without UK: 161 +/- 31; with UK 325 +/- 21 microliters/100 g body wt/min). This UK 38485 effect on GFR was no longer detectable at 24 hours, two days and seven days. Initiation of glomerular immune injury was followed by significant proteinuria which averaged 250 +/- 85 mg/24 hr at day two. UK 38485 treatment, which reduced TxB2 formation in isolated glomeruli by 90% did not influence proteinuria. These data demonstrate that induction of heterologous, in situ immune complex glomerulonephritis stimulates glomerular thromboxane B2 formation, an effect which partially modulates the decrease in GFR at two hours. Thromboxane, however, does not seem to play a role in the mediation of proteinuria in this animal model.

Animals↗