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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.

Background: Several mechanisms in the body regulate the water transport within the cells up and down during physiological and pathological conditions. The discovery of aquaporins, water channel proteins, has brought more insight into and understanding of how water crosses plasma membranes within cells in body tissue., Material and Methods: The functions of aquaporins are not fully understood; this paper summarise current knowledge of various aquaporins., Results: Known aquaporins are discussed in relation to some physiological, pathological and clinical conditions., Interpretation: In the future, measurements of aquaporin concentrations in urine and possibly in other samples will give us a broader picture of water exchange and a better understanding of the mechanisms underlying water production in clinical states like renal and heart failure and liver insufficiency. Moreover, by manipulating water channel proteins by compounds developed for this purpose, one may have a tool for treating some clinical disorders in which water depletion or water overload is an important factor.

The heavier work load for qualified nephrologists in Norway over the last ten years is described and compared with the number of positions. The increase in the number of dialysis treatments, care of renal transplant patients and other tasks performed by qualified nephrologists is roughly doubled from 1985 to 1995. By contrast the number of employed qualified nephrologists to pursue the work has only increased by 20% over the same period. As of today there is a lack of capacity to educate new nephrologists to fill up forthcoming vacancies. When the actual need for nephrologists is taken into account, the discrepancy is much more serious and will become even more so over the next ten years if no immediate action is taken. We suggest the establishment of six new educational positions. Altogether, these six new positions will provide the capacity to educate a reasonable number of trained nephrologists to meet future challenges, to the benefit of patients.

Hypertension is a common finding in patients with renal parenchymatous diseases. Development of hypertension causes increased proteinuria, decline in glomerular filtration rate and reduced life span in experimental models of glomerulonephritis. Hypertension has been shown to reduce glomerular filtration rate in man. It is therefore important to treat hypertension. The blood pressure should be reduced to about 140/80 mm Hg. Reduction of glomerular capillary pressure, inhibition of glomerular permeability, renal hypertrophy and inhibition of mesangial metabolism are the main mechanisms of renal protection during antihypertensive therapy. Autoregulation of the renal blood flow probably has an impact on these mechanisms. Impaired autoregulation is found in kidneys with low glomerular filtration rate and during treatment with calcium channel blockers. Alpha receptor blockers, angiotensin converting enzyme inhibitors (ACE-) and angiotensin II receptor blockers do not interfere with autoregulation. All types of antihypertensive drugs provide similar renal protection when the glomerular filtration rate is reduced. When calcium channel blockers are used in kidneys with normal or slightly reduced function, either blood pressure should be kept strictly at normal levels or these type of drugs should be combined with ACE inhibitors or angiotensin II receptor blockers.

Malnutrition, shown by fat depletion and muscle wasting, is common in uremia. The methods used to describe body composition in uremia are controversial. We have used ultrasonography of the thigh to evaluate fat and muscle in haemodialysis patients (group 1) (n = 14), peritoneal dialysis patients (group 2) (n = 10) and normal controls (group 3) (n = 13). Musculus rectus femoris diameter (0.84 +/- 0.06 cm versus 1.15 +/- 0.08 cm, p < 0.05) and cross sectional area (3.0 +/- 0.4 cm2 versus 5.5 +/- 0.4 cm2, p < 0.01) were significantly reduced in group 1 compared with group 3, as was also muscle area in group 2 (3.9 +/- 0.6, p < 0.05), indicating malnutrition in the dialysis patients. Peritoneal dialysis patients tended to have more subcutaneous fat (p = 0.07) and a larger musculus rectus diameter (p = 0.09) than haemodialysis patients, possibly reflecting better preserved nutritional status. Ultrasonography was equal to computed tomography for estimating these parameters. Ultrasonography is a useful tool for evaluating body composition in uremia, and has a capacity for detection of malnutrition, and possibly for early discrimination between patient groups with different dialysis modalities.

Malnutrition and low serum albumin values predict increased mortality in uremic patients. Infrared interactance represents a novel approach to the estimation of body composition. We have examined total body fat, body water and fat-free weight in our male haemodialysis (n = 24) and peritoneal dialysis (n = 17) patients. There were no differences between the groups in a cross-sectional study. A longitudinal study showed a significant increase of total body fat (%) in the peritoneal dialysis patients after five months (mean values +/- SEM) (from 19.8 +/- 2.3 to 22.6 +/- 2.4, p < 0.05), and a significant decrease of body water (%) (from 59.9 +/- 1.5 to 58.2 +/- 1.6, p < 0.05). The difference in total body fat between the haemodialysis (n = 14) and peritoneal dialysis (n = 10) groups reached statistical significance (16.5 +/- 1.7 versus 22.6 +/- 2.4, p < 0.05). No difference was found in serum albumin. Infrared interactance has the capacity to characterize time-dependent differential changes of body composition in various dialysis modalities. Further studies are needed to describe the validity of the method for identification of patients with increasing malnutrition.

Alpha-receptor blockers reduce blood pressure by blocking of the alpha 1-receptors in the smooth muscle cells in the arteriolar walls. The heart pump function is not disturbed. Most studies have shown that the alpha-receptor blockers induce a reduction in plasma-triglycerides and an increase in the ratio between HDL- and LDL-cholesterol. They do not interfere with the metabolism of electrolytes, glucose or uric acid and have no negative effect on pulmonary function. Although long-term use does not induce a permanent increase in heart rate, some patients respond to initial therapy with faster heart rate and palpitations. The alpha-receptor blockers should not be used in patients with coronary heart disease if the patient is not on chronic beta-blockade. When these precautions are followed, the alpha-blockers can be used as first-line treatment--just like ACE-inhibitors and calcium-antagonists.

20 patients with rapidly progressive glomerulonephritis were treated at the nephrological section, Medical Department A, Haukeland Hospital from 1973 to 1988. Nine patients had an idiopathic type of nephritis, while seven patients had this type of glomerulonephritis secondary to systemic lupus erythematosus, endocapillary glomerulonephritis, Henoch-Schönleins purpura or Wegener's granulomatosis. Four patients had antibodies to glomerular basement membrane. All renal biopsies showed extracapillary proliferation and tubular cell damage. All patients were given immunosuppressive treatment with corticosteroids and cytotoxic drugs. Nine patients who were admitted to the hospital from 1973 to 1978 were not treated with plasmapheresis, 11 patients from 1978-1988 were all treated with plasmapheresis. After one year of observation, six of the nine patients in the first group had died, while this applied to only two in the group treated with plasmapheresis. Early diagnosis and plasma exchange, in addition to immunosuppression, seems to be the best treatment for these patients.

Three case histories are described which highlight some of the predisposing risk factors and therapeutic strategies in the event of acute severe renal failure during treatment with ACEI. With appropriate therapy, renal function is usually restored within a few days. Renal artery stenosis, dehydration and diuretics stimulate the renin angiotensin system and make preservation of normal renal function, increasingly dependent on angiotensin II. The prevalence of renal artery stenosis is substantially increased in patients with peripheral vascular disease or with coronary artery disease with concomitant hypertension. Patients should be told about the increased risk of adverse effects to the kidneys if they become dehydrated. In these cases it is essential to reduce the dose diuretics and ACEI, and it may be necessary to give parenteral fluid substitution.

Stimulation of the renin angiotensin system, catecholamines and antidiuretic hormone causes prominent vasoconstriction in severe heart failure. Angiotensin converting enzyme inhibitors reverse these effects, and thus ameliorate cardiac function and reduce mortality in severe heart failure. Angiotensin II is an important regulator of renal function in diseases with renal hypoperfusion, and treatment with angiotensin converting enzyme inhibitors may cause a serious decrease in glomerular filtration and hyperkalemia. Asymptomatic heart failure, acute heart failure and acute myocardial infarction are areas where angiotensin converting enzyme inhibitors may prove beneficial in the future.

During the period 1981-1986, membranoproliferative glomerulonephritis was demonstrated in ten patients admitted to the Medical Department, Haukeland Hospital. At the time of the diagnosis all patients had proteinuria and hematuria, and six of them had renal failure. Seven patients exhibited nephrotic syndrome and three patients developed progressive renal failure during the observation period. Three patients died during the follow-up period. Four patients were treated with Cyclosporine A and corticosteroids. With this therapy the proteinuria disappeared in two of the patients with nephrotic syndrome. Immunosuppressive treatment may be tried if the disease shows signs of progression. We believe that some of these patients may benefit from cyclosporine A.