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Biomedical subjects

B Grabensee

Publications and source records attributed to B Grabensee.

At least 109 records · Page 6Linked to original sources
PubMed1996

[Automatic peritoneal dialysis--an adequate therapy option for the treatment of terminal kidney failure. First experiences with a new, pneumatically operated cycler].

OBJECTIVE: To determine whether (1) the recently developed pneumatic cycler for automatic peritoneal dialysis (APD) achieves individually adjustable adequate dialysis efficacy, and (2) changing from continuous ambulatory peritoneal dialysis (CAPD) to APD results in an appropriate increase of dialysis efficacy. PATIENTS AND METHODS: Between July 1994 and August 1995 dialysis treatment for chronic renal failure was performed in 17 patients (four women, 13 men: mean age 42.9 +/- 11.6 years). Ten patients decided primarily on APD, seven changed over from CAPD to APD because of inadequate dialysis efficacy. Adequacy of dialysis was judged by clinical criteria, weekly creatinine clearances (wCcr) and urea levels (urea elimination related to distribution volume [wKT/V]). RESULTS: Mean treatment period with APD was 7.9 +/- 0.3 hours, dialysate volume 19.4 +/- 2.3 1. An ultrafiltration of 1253 +/- 643 ml was achieved. Mean serum creatinine was 13.1 +/- 3.5 mg/dl, mean serum urea-nitrogen 61 +/- 15 mg/dl. wCcr was 78.6 +/- 27.2 1, wKT/V 2.21 +/- 0.33. All patients were adequately dialysed with various forms of APD. In those patients who changed from CAPD the dialysis efficacy, judged by weekly urea-nitrogen elimination, increased by 50% from 1.42 +/- 0.29 to 2.14 +/- 0.20 (P < 0.05). With the pneumatic cycler the different dialysis modes were achieved without problem. CONCLUSION: APD with the new pneumatic cycler provided an adequate and attractive option, from both medical and psychosocial aspects, in the dialysis of patients in chronic renal failure. Changing from CAPD to APD in certain patient groups clearly increased dialysis efficacy so that changing over to haemodialysis can often be avoided.

Adult↗
PubMed1996

[Cardiosurgical therapy of coronary heart disease in terminal kidney insufficiency].

OBJECTIVE: To determine retrospectively the complications and long-term results of aortocoronary bypass grafting in patients with end-stage renal disease. PATIENTS AND METHODS: 65 patients with coronary heart disease (CHD) and on dialysis (54 men, 11 women; average age 56.9 +/- 8.1 years) underwent aortocoronary bypass grafting between 1982 and 1992. Mean duration of dialysis (haemo- or peritoneal) was 41.1 +/- 45.0 (1-215) months. All patients had had haemofiltration treatment in conjunction with the bypass operation. RESULTS: Coronary angiography demonstrated triple-vessel disease in 40 patients (62%). Average number of bypasses was 2.8 per patient. Perioperative death rate was 4.6%. 95% of survivors were free of symptoms 6 months postoperatively. Long-term survival rate was 71% after 3 years and 55% after 5 years. CONCLUSION: Aortocoronary bypass grafting for CHD in patients with end-stage renal disease can be performed with a low perioperative mortality rate and significantly improves symptoms.

Adult↗
PubMed1996

Association of primary renal non-Hodgkin's lymphoma with mesangioproliferative glomerulonephritis.

A 27-year-old male developed nonoliguric renal failure. Renal biopsy of the left kidney showed infiltration by a diffuse large-cell non-Hodgkin's lymphoma (NHL). Laparoscopy, CT scans of the abdomen and thorax, and bone-marrow biopsy revealed no further manifestations of lymphoma. Primary renal NHL was diagnosed. The patient attained complete remission with cyclophosphamide, adriamycin, vincristine, and prednisone (CHOP) chemotherapy and remained disease-free for 13 years. Eight years after his first presentation, the patient developed acute oliguric renal failure with nephrotic syndrome. Mesangioproliferative glomerulonephritis was diagnosed in a biopsy of the left kidney. Chronic hemodialysis was required until cadaver kidney transplantation was successfully performed 5 years later. Although the association of NHL and glomerulonephritis has been described several times before, to our knowledge this is the first report of glomerulonephritis in primary renal lymphoma.

Adult↗
PubMed1996

Long-term clinical course in acute crescentic glomerulonephritis.

If non-treated or misdiagnosed, acute crescentic glomerulonephritis, clinically defined as rapidly progressive glomerulonephritis (RPGN), may lead to end-stage renal failure (ESRD) within a short time. Histologically, it is characterized by accumulation of inflammatory cells in combination with proliferation of epithelial cells in the glomerulus. According to the proposed immunopathogenic classification by Couser [7], predominantly the immunopathogenic type III without immune deposits often represents the renal manifestation of a systemic vasculitic disease, e.g. polyarteriitis or Wegener's granulomatosis. Having investigated 75 patients with acute crescentic glomerulonephritis for long-term results, we concluded that early histopathologic diagnosis by using an activity and chronicity score system may be not only a predictor for renal prognosis but also a valid supposition for differentiated immunosuppressive therapy in supplement to the clinical data on renal function. The therapeutic advantage of plasmapheresis therapy in addition to immunosuppressive therapy could not be proven.

Acute Disease↗
PubMed1996

The German Glomerulonephritis Therapy Study: 10 years of controlled randomized trials for the treatment of idiopathic glomerulonephritis.

The German Collaborative Glomerulonephritis Therapy Study, which celebrated its 10th anniversary in 1996, has collected data on more than 1,000 patients with biopsy-proven glomerulonephritis. 929 patients could be evaluated and 500 were treated according to at least one of various protocols developed for a randomized controlled trial. Current results show that prednisolone is effective in minimal-change nephropathy, and in combination with other immunosuppressants it can reduce proteinuria in individual cases of focal and segmental glomerulosclerosis, membranous glomerulonephritis and nephrotic IgA nephropathy. The majority of tested treatment protocols did not prove to be superior to symptomatic therapy for long-term outcome.

Adolescent↗
PubMed1996

Atrial natriuretic peptide in renal transplantation.

Factors related to atrial natriuretic peptide (alpha-ANP) regulation and its potential impact on excretory transplant function were examined in a prospective cohort study of 20 patients with end-stage renal disease over 21 days after allogenic kidney transplantation. Depending on posttransplant graft function, patients were separated into those with primary renal function (PF group, n = 10) and posttransplant acute renal failure (ARF group, n = 10). ANP concentrations were markedly elevated in both PF and ARF immediately after renal transplantation, even when compared with the pretransplant dialysis phase (PF group: 939 +/- 467 pg/ml; ARF group: 648 +/- 306 pg/ml, on 3rd postoperative day; "normals': 72 +/- 35 pg/ml). Whilst ANP levels were persistently elevated in patients with acute renal failure, there was a steady decrease in plasma concentrations in patients with primary renal function (PF: 270 +/- 122 pg/ml on 21st day). ANP concentration correlated with endogenous creatinine clearance (rz = 0.56, p < 0.01, PF group). Moreover, there was a greater correlation between ANP levels and postoperative hydration status, measured as central venous pressure or the difference from predialysis dry weight (rz = 0.79 and rz = 0.74, p < 0.01, PF group). Systolic blood pressure was also positively correlated with ANP concentrations. Together, these factors accounted for a total correlation coefficient of r = 0.87 (p < 0.001) in multiple regression analysis. No significant relation was found between plasma ANP levels and total or fractional sodium excretion or free water clearance. With the restoration of renal function most vasoactive hormones (renin-aldosterone system, catecholamines, vasopressin) decreased towards normal values, whilst ANP plasma concentrations remained elevated.

Adult↗
PubMed1996

Tubular dysfunction following kidney transplantation.

After transplantation the kidney is subjected to rejection and other deleterious factors including ischemic damage, acute tubular necrosis, rejection and the use of cyclosporine A (CsA) or FK506. As a result, kidney damage may be generalized with azotemia as its hallmark. These tubular syndromes may cause profound changes in the acid base balance and in the level of certain blood electrolytes and minerals. As a general rule, the renal tubular acidosis (RTA) that appears early following transplantation disappears spontaneously and is predominantly a sequela to acute renal failure. On the other hand, defects occurring in the late posttransplant period are often due to chronic rejection or CsA-induced nephrotoxicity. Secondary hyperparathyroidism, urinary tract infection and obstructive uropathy may also play a contributory urinary role in the pathogenesis of RTA. Chronic RTA following transplantation may interfere with bone metabolism and at times lead to nephrocalcinosis and nephrolithiasis. Therefore, if the condition is prolonged, a supplement of bicarbonate should be given if for no other reason that to protect the skeleton. As these patients may develop either hyperkalemia or hypokalemia, treatment with potassium supplements or potassium-sparing diuretics should be carried out with caution and under constant surveillance. Furthermore, magnesium replacement may be advisable if hypomagnesemia by decreased proximal reabsorption becomes clinically evident. Tubular dysfunction may occur following renal transplantation even in patients with maintained glomerular filtration rate and may induce a number of clinical problems including deterioration of renal graft function.

Humans↗
PubMed1996

Acute blockage of the renin system and differential renal vein renin determinations in the diagnosis of renovascular hypertension.

For validation of differential renal vein renin determinations in the diagnosis of renovascular hypertension (RVH), we investigated 102 patients suspected of suffering from RVH before and 1 h after administration of 25 mg captopril. Sensitivity, specificity and posterior probability for renin ratio (RR) and renin secretion (RS) were calculated based on 44 patients with proven RVH and 58 patients with primary hypertension (PH) using discriminant analysis. There is good (> 95%) and identical specificity of both variables under all conditions, whereas sensitivity remains poor even after Captopril administration (RR 23% vs. 32%; RS 20% vs. 34%). The posterior probabilities obtained by discriminant analysis revealed a cut-off point of 2.5 for the renin ratio and of 1.9 for the renin secretion. No change is observed after ACE inhibition. We conclude that the acute blockade of the renin system by captopril in differential renin sampling yields no advantages in diagnosing RVH and that there is no difference between RR and RS in the diagnosis of RVH.

Adult↗
PubMed1996

Atrial natriuretic peptide, sodium retention, and proteinuria in nephrotic syndrome.

BACKGROUND: Oedema formation in the nephrotic syndrome is primarily due to tubular sodium retention. The pathogenetic role of alpha atrial natriuretic peptide (ANP), a hormonal promoter of natriuresis is unknown. METHODS: In 31 patients (aged 35+/-11 years) with nephrotic syndrome and histopathological evidence of primary glomerulonephritis, we investigated plasma ANP concentration and its influence on renal haemodynamics, natriuresis, and proteinuria (total protein, albumin, IgG excretion). Patients with a compensated treated form of nephrotic syndrome due to primary glomerulonephritis were included in the study. Serum creatinine levels were <=1.4 mg/dl. Diuretic medication was discontinued at least 24 h before the investigation was started. Patients were randomly assigned to ANP infusion (0.005 microg/kg*min; group II, n=15) or received placebo (group III, n=16). Ten healthy subjects (group I) served as normal controls. RESULTS: In normal subjects (group I), ANP caused an increase in natriuresis from 14.5+/-4.2 mmol/h to 26.4+/-11.1 mmol/h (P<0.01). In patients with nephrotic syndrome (group II), baseline sodium excretion of 10.5+/-6.0 mmol/h was increased to 19.6+/-14.8 mmol/h with ANP infusion (P<0.01). No changes were seen in the placebo group III. The absolute increase in ANP induced natriuresis was not significantly different between group I and II. However, plasma ANP levels were significantly higher in patients with nephrotic syndrome (166+/-87 pg/ml vs. 74+/-21 pg/ml, P<0.05) and also reached higher levels after ANP infusion (P<0.01). Therefore, natriuresis was significantly reduced when circulating ANP levels were taken into account (P<0.05). ANP administration resulted in an increase of total protein excretion in patients with the nephrotic syndrome (group II, from 219+/-277 mg/h to 264+/-268 mg/h). Albumin elimination rose from 128+/-151 mg/h to 167+/-170 mg/h (P<0.05) and IgG excretion from 4.91+/-6.67 mg/h to 9.27+/-10.78 mg/h (P<0.05). Healthy subjects also showed a small but significant increase in albuminuria (48+/-38%, P<0.05). Low-dose ANP infusion did not, however, induce any significant alteration in GFR, ERPF and blood pressure. CONCLUSION: ANP plasma concentrations in the steady state are elevated in patients with the nephrotic syndrome. The natriuretic effect of ANP is reduced when referring to circulating ANP plasma levels. Elevated ANP levels enhance urinary protein excretion in the nephrotic syndrome. This is not due to modulation of GFR or FF, but is most probably attributable to increased glomerular permeability.

Adult↗
PubMed1995

Comparison between serum levels of bone alkaline phosphatase and the carboxy-terminal propeptide of type I procollagen as markers of bone formation in patients following renal transplantation.

The serum concentrations of the carboxy-terminal propeptide of type I procollagen (PICP) were monitored in 52 serum samples from 13 patients receiving renal transplants and the values compared with bone alkaline phosphatase (BAP) concentrations and intact parathyrin levels. There was a significant correlation between BAP and PICP values in all 52 serum samples examined (r = +0.770; P < 0.0001). Before transplantation BAP (P < 0.0001), but not PICP (P > 0.1), was correlated with intact parathyrin levels. BAP concentrations increased from 7.3 +/- 1.2 micrograms/l (median +/- S.E.M.) before transplantation to 13.3 +/- 1.2 micrograms/l 3 months after transplantation (P < 0.01). There was a concomitant rise in PICP levels from 95 +/- 19 micrograms/l to 166 +/- 27 micrograms/l (P < 0.05). No correlation was found between BAP or PICP levels on the one hand and intact parathyrin concentrations on the other at any time following renal transplantation (P > 0.5). In conclusion, PICP may be a useful parameter for monitoring bone formation following renal transplantation.

Adult↗
PubMed1995

[Doppler sonographic evaluation of the effectiveness of an antirejection treatment after kidney transplantation].

Data on 64 rejection reactions in 108 consecutive patients after renal transplantation (61 males, 47 females; mean age 42.8 +/- 12.9 years) were analysed to test what Doppler sonographic measurements can be used to predict whether a given drug regimen is able to suppress rejection. Results were compared with renal function and histological evidence of rejection. The >> pulsatility index << (PI), which is dependent on flow resistance, was determined by Doppler echocardiography: it increases on rejection (measurements made 2.0 +/- 1.1 days apart). The rejection reaction was successfully controlled by drugs (methylprednisolone, azathioprine and cyclosporin) in 44 patients (group 1), but not in 20 patients (group 2). PI before rejection (group 1: 1.8 +/- 0.5; group 2: 1.7 +/- 0.6), PI during histologically confirmed rejection (2.6 +/- 1.2 and 3.1 +/- 1.4, respectively), the size of difference between these values, and parameters of renal function provided no pointers to any drug efficacy in suppressing rejection. But individual changes in PI during suppression treatment proved to be of outstanding value (P < 0.00005). Signs of florid rejection at the end of treatment period correlated with a rising PI in 13 of 17 rejection episodes, while PI fell in only 7 of 47 episodes. Vascular signs of rejection tended to be poor predictors of rejection (P .028). - These findings indicate that serial Doppler sonography can be helpful in monitoring antirejection treatment.

Adult↗
PubMed1995

Monitoring of bone resorption after renal transplantation by measuring the urinary excretion of pyridinium cross-links.

The urinary excretion of pyridinium cross-links was measured in 70 second morning urine samples from 49 patients following renal transplantation. One and three months after renal transplantation, the urinary excretion of pyridinium cross-links was higher (p < 0.05) than at one week after transplantation. At all times after transplantation, the values for the excretion of pyridinium cross-links were correlated with the bone alkaline phosphatase concentrations (p < 0.001). However, there was no correlation between parathyrin concentrations and the values for the excretion of pyridinium cross-links (p > 0.05). This rise in the excretion of pyridinium cross-links is probably due to an increase of bone resorption caused by cyclosporin A and/or glucocorticoids. In the case of 17 urines with excretion values of pyridinium cross-links above the upper reference limit (pyridinoline equivalents, 93 mumol/mol creatinine), only 2 (12%) of the corresponding sera showed increased bone alkaline phosphatase values. In patients following renal transplantation simultaneous assessment of bone formation and bone resorption (determined from bone alkaline phosphatase serum concentrations and the excretion of pyridinium cross-links) may therefore enhance the diagnostic sensitivity for detecting effects on bone metabolism.

Adult↗
PubMed1994

[A hemolytic crisis with liver failure as the first manifestation of Wilson's disease].

An 18-year-old woman developed an acute haemolytic anaemia, acute transient renal failure and progressive hepatic failure. Coeruloplasmin and serum copper concentration were normal; a Kayser-Fleischer ring and any neurological symptoms were absent initially. Liver biopsy was contraindicated because of increased bleeding tendency. Wilson's disease was diagnosed only after the acute renal failure had regressed, on the basis of the urinary copper excretion (2890 micrograms/d, rising to 7330 micrograms/d after D-penicillamine administration). Progressive liver failure required transplantation. After it the patient quickly recovered and is now, two years later, free of disease. -This case demonstrates that Wilson's disease may be difficult to diagnose at the time of initial acute manifestation. But it can be recognized early from the pathognomonic low alkaline phosphatase and by calculation of free serum copper.

Acute Disease↗