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A wide spectrum of acute or chronic heart failure and thromboembolic events may be causally related to high-grade uni- or bilateral renovascular hypertensive disease, and the variety of these potential interactions may be unrecognized in clinical practice. We present three cases that illustrate the clinical variability of cardiorenal failure and thromboembolic events seen in patients with significant renal artery stenoses. These are high-risk patients where severe morbidity and mortality are threatening. Our patients also demonstrate that the diagnosis often is delayed, and that recanalizing of occluded renal arteries may be highly cost-effective and life-saving in such patients. [ABSTRACT FROM AUTHOR]

We describe a man and a woman with Fabry's disease. Renal biopsies showed late and early stages respectively of focal and segmental glomeruloscierosis (FSGS) and vascular changes. Clinically the hemizygous patient had advanced renal disease with nephrotic range proteinuria and serum creatinine 122 μmol/l. The female carrier had minimal albuminuria, borderline GFR with a normal serum creatinine, acroparesthesias, moderate fatigue, tinnitus and headache accompanied by ischemic cerebral lesions. Enzyme replacement therapy (ERT) was initiated according to our Fabry protocol, partly due to the renal morphologic findings. We conclude that FSGS and vascular changes may be an early morphologic finding in Fabry's disease, even in patients with subtle albuminuria. The potential role of FSGS as a marker of progressive renal disease in some Fabry patients is discussed. As FSGS and vascular changes obviously may exist across a wide range of clinical presentations and have potential prognostic implications, we suggest that a renal biopsy should be performed prior to enzyme replacement therapy in all adult Fabry patients with proteinuria of various levels. Efforts should be made to develop a scoring system to evaluate potential histologic markers. Protocol biopsies may have therapeutic implications and may provide valuable information in the evaluation of start and dosing of ERT. [ABSTRACT FROM AUTHOR]

Objective: The renal functional consequences of an activated sympathetic nervous system and plasma atrial natriuretic hormone (ANP) in various renal diseases are not well described. We hypothesize that norepinephrine (NE) and ANP have antagonizing effects on renal hemodynamics in diseased kidneys. Material and Methods: Plasma NE, ANP, glomerular filtration rate (GFR), effective renal plasma flow (ERPF) and mean arterial pressure (MAP) were measured in the upright position in healthy controls (n = 9) and hypertensive patients with reduced GFR (n = 11). The same parameters were compared between healthy controls (n = 6) and hypertensive patients with reduced GFR (n = 6) in upright and supine positions. Results: Upright plasma NE and ANP were significantly elevated in the patients compared with the controls (4.4 ± 0.4 vs 2.1 ± 0.2 nmol/l (p < 0.001) and 13.5 ± 2.1 vs 6.9 ± 1.0 nmol/l (p < 0.01) respectively). With change from upright to supine position plasma NE decreased in the controls (2.2 ± 0.3 vs 1.7 ± 0.3 nmol/l) (p < 0.01) and patients (3.8 ± 0.4 vs 2.6 ± 0.4) (p < 0.01). Supine ANP increased in controls (5.5 ± 1.0 vs 8.3 ± 1.1) (p < 0.01) but not in patients (14.3 ± 3.8 vs 16.1 ± 3.8 nmol/l) (p > 0.10). Plasma NE correlated positively with MAP (p < 0.001) and negatively with GFR (p < 0.01) in the upright but not supine position. A positive correlation between NE and ANP was observed in upright (p < 0.001) but not in supine position. ANP correlated negatively with GFR in the upright (p < 0.01) but not supine position. No position dependent changes were seen in GFR and ERPF, but supine filtration fraction (FF) increased insignificantly in the patient group (0.23 ± 0.02 vs 0.24 ± 0.02) (p < 0.05). Conclusion: Hypertensive patients with reduced GFR have elevated levels of plasma NE and ANP in the upright body position. When the upright and supine positions are compared, plasma NE declines in the supine position in controls and hypertensive renal failure patients, and plasma ANP levels are elevated only in the upright position in hypertensive renal failure patients where the sympathetic nervous system is activated. A significant positive relationship between plasma NE and ANP was observed only in the upright position. The upright body position seems superior to recumbency in the characterization of these hormonal changes in hypertensive chronic renal failure patients. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to quantitate inflammatory cells in renal biopsies from patients with Wegener's granulomatosis (WG) and to identify cells participating in early fibrogenesis. The goal was to determine whether these cells correlated with the severity of renal disease and whether their presence had a bearing on renal prognosis. Material and Methods: Sixty-one patients with WG who had a renal biopsy taken at the time of diagnosis were included in the study. Immunostaining with monoclonal antibodies towards macrophages (CD68), T- and B-lymphocytes, α-smooth muscle actin (α-SMA) and vimentin was done. Results: The dominating intraglomerular leucocytes were macrophages (29.9 ± 15 cells/glomerular cross-section) and to a lesser extent T-cells (2.57 ± 1.8 cells/glomerular cross-section). No B-lymphocytes were detected in the glomeruli. More than two-thirds of the T-cells were CD8[sup +] (cytotoxic) cells. Macrophages and T-lymphocytes were distributed equally in the renal interstitium and were numerous around crescentic glomeruli. Glomerular and interstitial macrophages and interstitial T-cells correlated significantly with serum (S-) creatinine at the time of biopsy but not after 1 year. S-creatinine at the time of biopsy and after 1 year differed significantly among the three levels of interstitial α-SMA staining. S-creatinine at biopsy was highest when tubular vimentin staining was strongest, and tubular vimentin staining was strongest in patients with acute tubular damage. Conclusions: Evidence was found for a cellular type IV immune response in WG, with CD8[sup +] T-lymphocytes and macrophages dominating the cellular infiltrate. The detection of interstitial α-SMA, probably staining myofibroblasts implicated in renal fibrogenesis, indicated a low glomerular filtration rate 1 year after renal biopsy. [ABSTRACT FROM AUTHOR]

An direct haemagglutinatiion (IHA) test using tanned sheep erythrocytes was developed to detect antibodies in sera from rabbits immunized with renal tubular epithelium (RTE) or with glomerular basement membrane (GBM) from rats. The RTE antigen preparation, called Fx1aA, sensitized the erythrocytes directly, whereas the GBM preparation had to be treated with collagenase. The antisera to Fx1A gave titres up to 64,000, and the antisera to GBM up to several million. The sera were monospecific, since they gave no cross-reactions in IHA, precipitation, or absorption tests. Using the IHA test, the quantitative aspects of experimental glomerulonephritis in rats can be studied. Preliminary results obtained in transfer experiments indicate a dose-response relationship between the titres in IHA and the degree of proteinuria. [ABSTRACT FROM AUTHOR]

Glomerular complement receptors (GCR) were demonstrated by the adsorption of C3 coated sheep erythrocytes to cryostat sections of human kidneys. An epithelial localization of the GCR is implied by the binding pattern of the indicator cells. The GCR activity was reduced in all glomeruli where in vivo deposition of immunoglobulin and C3 along the capillary wall was observed. In fourteen out of nineteen biopsies where deposits in the mesangium were seen, reduced GCR activity was also observed, whereas GCR activity was normal in the other five. Immunofluorescence and haemadsorption tests performed on the same section showed that C3 deposits corresponded to areas showing reduced complement receptor activity. Areas outside the C3 deposits adsorbed indicator cells coaled with various amounts of C3 similarly to the adsorption to glomeruli seen in normal adult and fetal kidneys. Sclerotic glomeruli showed no GCR activity. The results indicate that the complement receptors play a role for the binding of complement-containing complexes in glomeruli. [ABSTRACT FROM AUTHOR]

The renal effects of low-dose cyclosporin A (CsA) treatment in severe psoriasis was investigated in 10 patients treated with a mean CsA dose of 3.23 (range 1.94–4.10) mg/kg/day for 12 months. The psoriasis area and severity index was reduced by 63–76%. Ambulatory GFR (iothalamate-I) ERPF (hippuran-), RVR and MAP were examined at 3-months intervals. A control renal biopsy was performed shortly before treatment start and a second biopsy was taken after 12 months of therapy. GFR was slightly but significantly reduced after 6 and 9 months; after 12 months the decrease was not significant (121.0±7.6 versus 115.2±7.8 ml/min/l.73M >0.10). After 12 months serum creatinine increased from 82±4 to 94±7 μmol/litre (<0.05 while an insignificant increase of ERPF was seen and FF decreased from 0.29±0.01 to 0.26±0.01 (<0.05). MAP remained unchanged. GFR and serum creatinine correlated significantly within each 3-month interval. A slight interstitial fibrosis was seen in the second biopsy in 4 of 10 patients receiving a mean CsA dose of 3.2–4.1 mg/kg/day. In three of these patients a concomitant rise in serum creatinine was seen. In conclusion, low-dose CsA was associated with reversible fall in GFR and potentially progressive structural changes not always accompanied by corresponding functional alterations. One should consider reducing the daily dose of CsA to 3.0 mg/kg body- weight or less in CsA therapy up to 1 year. [ABSTRACT FROM PUBLISHER]

Complement receptors for C/C (CRI) on erythrocytes (ERC1) and renal glomeruli (GCR1) were examined in patients with different types of renal disorders. Normal ECR1 activity was found on erythrocytes from patients with IgA glomerulonephritis, benign nephrosclerosis and other types of renal diseases. In patients with systemic lupus erythematosus (SLE) and glomerulonephritis ECRl activity was low or absent in 75% of the patients. The GCR1 activity, however, was normal except in areas with complement deposits where GCR1 activity was abolished. During treatment with corticosteroids and azathioprine of patients with SLE the clinical response was followed by increased functional ECR1 activity. In those patients who did not respond the ECR1 activity was persistently low. Three patients with renal transplant all showed increased ECR1 activity. [ABSTRACT FROM PUBLISHER]

Background: Acute renal failure is a well-known complication in patients with renal artery stenosis during treatment with ACE inhibitor. Renal artery thrombosis after withdrawal of ACE inhibitor has not been reported previously., Material and Methods: We describe a patient with acute renal failure with an unexpected course., Results: A 67-year-old man was admitted with acute anuric renal failure during treatment with hydrochlorothiazide and enalapril. His blood pressure was 165/60 mm Hg. Renal ultrasound was normal. After initial rehydration and dialysis, diuresis resumed until a sudden unexpected anuric renal failure recurred on day 12. Angiography disclosed bilateral renal artery occlusion. The right renal artery was successfully opened and a stenosis was blocked and stented, and brisk diuresis ensued. Two days later hypertension accelerated, and a new invasive procedure on day 24 succeeded in opening, blocking and stenting a proximal stenosis in the left artery; a mobile thrombus was located behind the stenosis and successfully treated with intraarterial thrombolysis. Blood pressure rapidly normalized, and serum creatinine was normal on visits 1.5 and 4 months later., Interpretation: General aspects and prevention of acute renal failure during ACE inhibitor therapy are discussed. Acute renal thrombosis after withdrawal of ACE inhibitor in patients with stimulated renin angiotensin system and significant renal artery stenosis may be causally related to the antifibrinolytic effects of angiotensin II and aldosterone. Endovascular reconstruction of renal artery occlusion may completely restore the kidney function.

Background: The incidence of acute renal failure requiring dialysis is not known in our country. The criteria for acute dialysis are not uniformly accepted, neither is there consensus on dialysis strategy in critically ill patients. We describe the acute dialysis activity in our hospital in 1999., Material and Methods: We have retrospectively recorded the indications for dialysis and the course and hospital mortality in all patients treated with acute dialysis in 1999., Results: 108 patients were treated with 670 dialysis procedures; the incidence was 20.5 per 100,000 inhabitants. Continuous veno-venous haemodiafiltration accounted for 37% of all treatments. In 50% of the patients acute renal failure occurred after surgery or serious infections with a mortality of 57% and 62% respectively. Total dialysis mortality was 45%. The mortality in patients with malignancy and peripheral vascular disease was 90% and 75% respectively. 10% of the patients needed chronic dialysis., Interpretation: The incidence of acute dialysis was higher than previously reported from European countries and may be related to the general increase in active treatment of patients with complicated diseases. The mortality rates are persistently high. Close cooperation between nephrologists and intensivists in the treatment of these patients is essential.