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Most renal cell carcinomas coexpress vimentin and keratin, while renal tubular epithelia express only keratin. Investigation of the intermediate filament composition of tubular epithelia in diseased rat and human kidneys now shows that altered tubular epithelia unequivocally coexpress keratin and vimentin. In rats, pronounced coexpression of vimentin and keratin was observed in chronic nephrosis induced by daunomycin, and the extent of coexpression seemed to increase with the incidence of altered collapsed and cystically dilated tubules and with the degree of tubular epithelial proliferation. It was also seen during tubular regeneration after acute tubulotoxic injury induced by mercury chloride poisoning, with vimentin expression being lost in fully regenerated tubular epithelium. In man, expression was seen in chronically and irreversibly damaged kidneys. Thus, vimentin can be expressed temporarily in acutely and reversibly damaged kidneys and chronically in irreversibly damaged kidneys. Vimentin could perhaps be regarded as an indicator of the regenerating and proliferating activity of tubular lesions.

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.

The cardioplegic solution HTK of Bretschneider was used for canine kidney protection. The kidneys were perfused with this solution for 6-10 min prior to the induction of ischemia. The kidneys were left in-situ for 60, 90, 120 and 135 min ischemia time at a temperature of 25-34 degrees C (n = 13). As a control group we used unilateral nephrectomized dogs (n = 9). After unilateral nephrectomy an elevated plasma creatinine in comparison to preoperative values was observed. After 60 and 90 min under HTK-protection the postoperative plasma creatinine was not elevated compared to the control group. After 120 min of ischemia creatinine level was slightly increased to an average of 2.1 mg% on the first and second postoperative day. These experiments indicate the protective effect of the cardioplegic solution for canine kidney preservation in situ.

The cardioplegia solution, HTK (histidine-tryptophan-ketoglutarate) (Bretschneider et al. 1975, 1984; Bretschneider 1980), was primarily developed to improve myocardial protection, as compared with periods of ischemia, during artificial cardiac arrest in open heart surgery. It has since become a routine clinical procedure (Preusse et al. 1987). According to our results, this solution also significantly improves ischemic tolerance of kidneys (Kallerhoff et al. 1985a, b, 1986, 1987c). The superiority over simple ischemia or over the Euro Collins solution holds for “cold” as well as for “warm” ischemia (Kallerhoff et al. 1988a). Renal ischemic tolerance was increased from 15–20 min to 2 h at normothermia (Kallerhoff et al. 1986). There have now been several clinical applications of this method (Blech et al. 1988; Kallerhoff et al. 1988b).

In order to improve dog kidney perfusion in situ with a protective solution, a perfusion catheter was constructed which allowed continuous pressure measurement in the center of the catheter tip during perfusion. Using this catheter, the equilibration of the extracellular space with a protective solution (HTK solution) was found to be pressure dependent. Continuous pressure and resistance control is therefore a prerequisite for reliable organ protection.

After a single oral dose of 4 mg/kg indomethacin (IDM) to sodium and volume depleted rats plasma renin activity (PRA) and systolic blood pressure fell significantly within four hours. In sodium repleted animals indomethacin did not change systolic blood pressure (BP) although plasma renin activity was decreased. Thus, indomethacin by inhibition of prostaglandin synthesis may diminish the blood pressure maintaining effect of the stimulated renin-angiotensin system in sodium and volume depletion.

Protection-methods, for an improvement of ischemic tolerance of the kidney, can be investigated by intraischemic analysis of metabolism and structure. A definite proof for the effectiveness of a protection method is only postischemic function in combination with postischemic structure-regeneration. For this reason postischemic function was chosen for examination of the protective ability of the Euro-Collins-solution and the HTK-solution during a two-hour reperfusion period. We perfused 57 dog kidneys either with the Euro-Collins- or with the HTK-solution prior to ischemia. Ischemia was 7, 60, 90 and 120 min after Euro-Collins-perfusion and 7, 120, 150 and 180 min after HTK-protection. The protected and ischemic kidneys were left in-situ; the mean ischemic temperature was therefore 20-25 degrees C for the shorter ischemic times and 30-34 degrees C for the longer ischemic times. We compared the protected and ischemic kidneys with 14 untreated kidneys (control). Postischemic renal blood flow (RBF) was measured by an electromagnetic flow probe; renal oxygen consumption (V02/min) was calculated by arterio-venous oxygen content difference and the renal blood flow. If urine could be collected, the glomerular filtration rate (GFR) was measured by an endogenous creatinine clearance. In Euro-Collins-protected kidneys after 60-120 min ischemia the RBF was after 15 min of reperfusion between 20 and 100 ml/min/100 g. After 30 min we got values of 100-200 ml/min/100 g. The V02/min, which was in the control kidneys between 5-6 ml/min/100 g, was about 2 ml/min/100 g.(ABSTRACT TRUNCATED AT 250 WORDS)

The morphological consequences of acute or chronic renal ischemia may consist of an anemic kidney infarction, bilateral cortical necrosis, acute tubular lesions in circulatory renal failure, so-called subinfarction, as well as arteriosclerotic endstage kidney. In renal biopsies obtained from patients with acute renal failure, renal dysfunction can be morphologically explained by acute intra- and extracapillary necrotizing glomerulonephritis in 50% of cases, and by solely acute tubular lesions in 30% of cases. It is suggested that the development of acute tubular lesions during circulatory insufficiency might be favoured by an angiotensin II-dependent vas efferens constriction, leading to a reduction of peritubular blood flow in the presence of preserved glomerular filtration. The balance between demand and supply of oxygen within the tubular epithelial cells might thereby be critically disturbed.

Kidneys were perfused either with Euro-Collins-solution or with HTK-solution of Bretschneider. The perfusion pressure as well as the perfusion flow were measured during a six-minute perfusion. The perfusion resistance was higher in Euro-Collins-kidneys than during HTK-perfusion. The venous outflow of the kidney as well as the ureteral outflow was measured during each minute of the perfusion and has analysed for osmolality, and for sodium and potassium concentrations. In Euro-Collins-kidneys a complete "equilibration" of the extracellular space was not achieved, while during HTK-perfusion concentrations in the venous as in the tubular outflow, similar to those in the HTK-solution itself, could be reached. At the end of the different perfusions, tissue was analysed for biochemical parameters such as ATP, ADP, AMP and lactate as well as for morphological features. Lactate had increased and ATP had decreased during perfusion with Euro-Collins-solution, while ATP had not changed and lactate had decreased during perfusion with HTK-solution. Normal glomerular, tubular and dilated vascular structures can be seen after HTK-perfusion, while a glomerular and vascular contraction takes place during Euro-Collins-perfusion.

The effect of the cyclooxygenase inhibitor indomethacin (3.4 mg/kg/24 hr) on systolic blood pressure (PB) and plasma-renin-activity (PRA) was evaluated in normotensive and renovascular hypertensive rats receiving either a normal or low salt diet. Indomethacin reduced PRA in normal and hypertensive animals on both low and normal salt intake. Indomethacin furthermore, decreased BP in animals on low sodium diet but increased PB in sodium repleted rats. These data suggest that the effect of indomethacin on rat BP may depend on the state of extracellular volume and PRA.

In 110 canine kidneys, we examined the time course of energy rich phosphates, lactate, intrarenal ph and renal morphology with Euro-Collins- or with HTK-protection of Bretschneider and compared these findings with unprotected kidneys during complete ischemia at 1 degree C and at 25 degrees C. Both kidney protective solutions prolonged energy-rich phosphate-decline by a factor of 3-4 compared with that of unprotected kidneys. The lactate increase was greater in Euro-Collins-protected kidneys than in HTK-protected and in unprotected kidneys, leading to pH values of 6.5 in Euro-Collins and to 6.4 in unprotected kidneys after 24 hours, in contrast to a pH-value of 7.3 with HTK-protection. This may be the reason for structural deterioration seen in unprotected and in Euro-Collins-protected kidneys after 12, and 48 h of ischemia at 1 degree C, whereas in HTK-protected kidneys a sufficient preservation of structure can be seen. In one human kidney, protected with Euro-Collins-solution, we were able to show that at 1 degree C intrarenal pH and lactate accumulation is similar to the levels in canine kidneys. In Euro-Collins preserved kidneys lactate accumulation at 25 degrees C is even greater than at 1 degree C, leading to inhibition of energy metabolism and to structural deterioration, whereas HTK-solution, because of its high buffer concentration, is able to maintain ischemic metabolism leading to sufficient protection of intrarenal pH and of adenine nucleotides as well as structural protection at 1 degree C and at 25 degrees C.

Eine Organschadigung durch Ischamie kann im Tierexperiment an einer Verschlechterung der energetischen Situation, an einer Storung der morphologischen Integritat und an einer postischamischen Funktionseinschrankung objektiviert werden. Dementsprechend mus sich ein gunstiger Einflus organprotektiver Masnahmen an diesen Kriterien — Energetik, Struktur und Funktion — aufzeigen lassen. Die Kardioplegische Losung HTK nach Bretschneider wirkt anerkanntermasen am Myokard gegenuber Ischamie protektiv — sowohl in energetischer wie auch in struktureller und funktioneller Hinsicht (Bretschneider et al. 1981; Gebhard et al. 1984; Preusse 1982; Schnabel et al. 1983).

Reduction of renal mass in the rat results in an increased glomerular prostaglandin (PG) and thromboxane (TX) formation that modulates renal hemodynamics. To evaluate whether dietary protein intake could exert effects on renal PG and TX formation after reduction of approximately 70% of renal mass, rats with remnant kidneys were placed on either a high-protein (HP) or a low-protein (LP) diet. After 2 wk on the diet, proteinuria, glomerular filtration rate (GFR), urinary PGE2 excretion, and glomerular PGE2, 6-keto PGF1 alpha, and TxB2 biosynthesis were significantly greater in the rats on HP diets. Two-wk administration of the thromboxane synthesis inhibitor UK 38485 reduced renal TxB2 formation by approximately 70%. In addition, chronic UK 38485 treatment significantly inhibited papillary PGE2 production. Neither chronic nor bolus administration of UK 38485 had an effect on proteinuria or GFR in rats on HP diets. Chronic UK 38485 treatment, however, reduced GFR and proteinuria in rats on LP diets. The bolus administration of UK 38485 did not alter GFR in animals receiving a LP diet. The cyclooxygenase inhibitor indomethacin reduced GFR only in rats on HP diets. The data demonstrate that HP intake stimulates renal prostanoid formation. The increased prostaglandin formation on HP intake modulates GFR in these rats.

A 74-year-old woman with refractory congestive heart failure due to long-standing calcific mitral stenosis who refused surgical intervention was treated with percutaneous balloon valvuloplasty. After an uneventful procedure, hemodynamic results were satisfactory with an increase in the mitral valve area from 0.4 to 1.1 cm2. Five hours after the procedure, the patient had a bout of vomiting followed by pulmonary aspiration. Electrocardiography, and in the further course, creatine kinase MB elevation, showed anterior myocardial infarction. Necropsy disclosed embolic material in the mid left anterior descending artery which unequivocally consisted of valvular material. This case demonstrates embolism of valvular debris as a life-threatening, procedure-related complication of percutaneous valvuloplasty of calcific mitral stenosis.

The first clinical use of Bretschneider's HTK-solution for in-situ-protection of the kidney in mild hypothermia is reported. By means of this protective method renal surgery can be performed in a bloodless field without permanent loss of renal function. After initial protective perfusion of the kidney no repeated perfusions or additional surface cooling must be done. There are no systemic side effects when the HTK-solution is applied appropriately.

Cyclosporin A (50 mg/kg orally for 7 days) produced severe degranulation and hydropic degeneration of islet B cells in rats. These changes were accompanied by hyperglycaemia and hypoinsulinaemia, while the pancreatic insulin content decreased by 75%.

Mit der Entgegennahme einer Gewebsprobe ubernimmt der Pathologe die Verantwortung, moglichst alie in einem solchen Biopsat potentiell enthaltenen, fur die Erkennung von Krankheiten wichtigen Informationen unter Einsatz von zeitgemasen morphologischen Methoden zu erf assen und auf dieser Grundlage eine rationale pathologisch-anatomische Diagnose zu formulieren. In begrundeten Fallen hat dies innerhalb weniger Stunden zu erfolgen. Daruberhinaus durfen von der Nierenbiopsiediagnostik Angaben zur Akuitat und zur Prognose eines Krankheitsprozesses erwartet werden.

Expression of villin, a 95-kd F-actin bundling and severing protein, is restricted in animal tissues to epithelial cells with a brush border. Thus, the enterocytes of the intestine and epithelial cells of proximal but not distal tubules of the kidney are strongly positive. Here we report a similar staining pattern for human intestine and kidney. In four human colon adenocarcinomas villin expression was seen in tubular and glandular structures but not in the undifferentiated parts. Fourteen human renal carcinomas (9-Grade I and 5 Grade II) were villin-positive, and 2 sarcomatous renal carcinomas (Grade III) were villin-negative. The percentage of tumor cells that were villin-positive varied from 10-90% for the Grade I and II types. Our results indicate that villin may be a grading marker that deserves further study in renal carcinoma. They also raise the question whether the majority of renal carcinomas are derived from the proximal tubular epithelium rather than from the distal epithelium.

The most frequent form of nephrosclerosis in human kidneys is the so-called benign variant. It may develop subsequent to even short-lasting hypertensive episodes. The interlobular arteries may be primarily affected, occasionally accompanied by glomerular and tubulointerstitial lesions. Consequently, progressive renal damage may occur potentially aggravating renal diseases of different origin. Malignant nephrosclerosis became a rare disease. Experimentally, it was impossible to induce its early intimal changes exclusively by high blood pressure values. Therefore, it was assumed that previous adaptive vascular changes, in addition to further advancing hypertension, may also be prerequisites for the development of malignant nephrosclerosis.

Veno-occlusive disease (VOD) developed in a 45-year-old white male 2 years after cadaveric kidney transplantation while receiving combined immunosuppressive therapy with prednisone and azathioprine. Early clinical signs at presentation included ascites and tender hepatomegaly. The diagnosis of VOD was established at laparoscopy and by histological examination of liver biopsies. Azathioprine was discontinued. Gross ascites refractory to medical treatment and decreasing liver function required surgical treatment by portacaval shunt. Transient postoperative complications were hepatic encephalopathy and considerable hyperbilirubinaemia. 8 months later the patient is well, with stable renal function and no clinical signs of hepatic disease.

Energy reserves (TAN) and anaerobic substrates (glucose, glycogen) are lower in renal than in myocardial tissue. Euro-Collins-solution contains nearly 200 mmol/l glucose, while the HTK-solution of Bretschneider contains none. Therefore the influence of glucose on kidney lactate production, on energy reserves (TAN), intrarenal pH and on morphology during the protection of ischemic kidneys was analysed using either Euro-Collins-solution, or modified "Euro-Collins-solution", containing mannitol instead of glucose, or HTK-solution with and without the addition of 5, 10 and 20 mmol/l glucose. Glucose content changed during kidney perfusion with Euro-Collins-solution from about 60 to 800 mumol/gdw. While intrarenal pH decreased from 7.1 to 5.1 in Euro-Collins-kidneys during 420 min of ischemia at 25 degrees C, pH decreased to 6.7 with the modified, mannitol containing "Euro-Collins-solution". In HTK-protected kidneys intrarenal pH decreased with increasing glucose addition to the solution. Although Total Adenine Nucleotides are highest at the end of ischemia with Euro-Collins-solution, structural protection after the same ischemic stress was best in HTK-protected kidneys without glucose addition. We conclude that glucose stimulated lactate production, reduced interstitial pH in the kidney even in combination with a highly buffered solution and that it might cause greater membrane permeability leading to a structural deterioration. Mannitol seemed more appropriate than glucose in this respect, although other substances, which provide energy substrate and prevent structural damage, may exist.

Experimental hydronephrosis in mice has been studied with histological, ultrastructural, immunohistochemical, biochemical, and electrophysiological techniques to establish its value as a preparation for the investigation of glomerular microcirculation as well as the electrophysiological and biochemical properties of the renin-containing juxtaglomerular (JG) and vascular smooth muscle (VSM) cells of the afferent glomerular arteriole. During developing hydronephrosis the kidney parenchyma becomes progressively thinner as a result of tubular atrophy, being, after 12 weeks, a tissue sheet of about 200 micron in thickness. In this preparation, the renal arterial tree, in particular the glomerular arterioles, and also the glomeruli can be easily visualized. This permits intravital microscopic studies or direct visual identification of JG and VSM cells for microelectrode impalement. In spite of complete tubular atrophy, the vascular system is well preserved. Ultrastructurally, JG and VSM cells as well as the axon terminals innervating the vessels are intact. The same holds for the glomeruli except for a certain confluence of the podocyte foot processes and a thickening of the basal lamina. Renin immunostaining and kidney renin content in the hydronephrotic organ correspond to those in control kidneys. In addition, renin release from this preparation can be stimulated in a typical manner by isoproterenol and inhibited by angiotensin II, indicating that the receptors controling renin release and the secretory mechanism itself are still intact. Electrophysiological recordings from JG and VSM cells show a high membrane potential (-75 mv), and spontaneous depolarizing junction potentials, owing to transmitter release from the nerve terminals. Inhibitors of renin secretion, e.g. angiotensin II, depolarize both cell types, whereas stimulators such as isoproterenol do not change the membrane potential. We conclude that the hydronephrotic mouse kidney is a suitable model for in vitro studies of the electrophysiology and biochemistry of the media cells of the afferent arteriole, as well as for in vivo studies of glomerular microcirculation.

In 1898 Tigerstedt and Bergman first detected the existence of renal renin and discussed its possible role in the development of cardiac hypertrophy associated with various kidney diseases. Hartwich (1930) and Goldblatt et al. (1934) were able to produce persistent arterial hypertension in dogs by narrowing the renal arteries. Subsequently, a large number of findings accumulated in the field of renal hypertension. Most of the material has been covered in reviews edited by Braun-Menendez (1946), Page and McCubbin (1968), and Page and Bumpus (1974). There is general agreement that arterial hypertension, including renal hypertension, is a multifactorial disorder of regulation as anticipated by Page in 1949 when he proposed his concept known as the mosaic theory.

Das Goodpasture-Syndrom wird haufig als eine Erkrankung definiert, die durch eine rapid progressive Glomerulonephritis mit diffuser Halbmondbildung und schnell zur Uramie fuhrender Niereninsuffizienz sowie haufig letal endenden Hamoptysen gekennzeichnet ist. Das es daneben auch Goodpasture-Syndrome ohne diffuse Halbmondbildung und ohne eine sich rasch entwickelnde exkretorische Niereninsuffizienz gibt, wird selten beobachtet und leicht verkannt. Unter 15 von uns beobachteten Fallen von Goodpasture-Syndrom haben wir zwei solche Falle beobachten konnen, deren Kasuistiken im folgenden dargestellt werden sollen.

Systolic blood pressure (BP) and plasma renin level (p.r.l.) were measured 1. in rats with chronic one-kidney-Goldblatt hypertension before, 1 1/2 h, 6 or 24 h after unclamping or sham-operation. 2. 6 h after 50 mg/kg furosemide i.p., and again 2 h after a subsequent nephrectomy. P.r.l. in the chronic stage of one-kidney-Goldblatt hypertension did not differ from that in normal control animals. Sham-unclamping did not influence BP and did not cause a significant increase of p.r.l. 1 1/2 h after unclamping BP fell considerably to still hypertensive levels while p.r.l. fell to less than half its normal value. 6 to 24 h after unclamping, BP continued to fall, while p.r.l. progressively rose to reach 78% of its normal value. Furosemide diuresis caused an increase of p.r.l., but no fall of BP. 2 h after subsequent nephrectomy p.r.l. fell to undetectable levels and BP to its normal value. The data suggest that the normal p.r.l. in the chronic stage of Goldblatt hypertension may be considered as inappropriate elevated in relation to blood pressure and sodium balance state due to partial protection of the kidney against regulatory influences by the presence of a clamp on the renal artery.

Earlier experiments have shown that in sodium depleted hypertensive rats with bilaterally constricted renal arteries the arterial pressure normalized after blockade of the renin-angiotensin system; simultaneously acute renal failure occurred. In hypertensive rats with unilateral renal artery stenosis an impaired excretory function of the clipped kidney can be expected, but may not be detectable by conventional tests of renal function. Male Wistar rats with chronic two kidney, one clip hypertension were fed a low sodium diet. After 7 days the rats were treated with vehicle, with the vasodilator dihydralazine, or with the angiotension converting enzyme inhibitor MK 421 for 2 weeks. During the 14-day treatment period a continuous blood pressure reduction was achieved in dihydralazine and MK 421 treated rats. Overall excretory kidney function (plasma creatinine concentration) was well maintained in all three groups until the end of the antihypertensive drug treatment. At the end of drug therapy mean glomerular filtration rates of the left clipped kidneys were significantly lower in both treated groups compared to hypertensive controls, and mean glomerular filtration rate of the left clipped kidneys of dihydralazine treated rats was significantly higher than in MK 421 treated rats: controls (N = 6) 1.03 +/- 0.03, dihydralazine-group (N = 10) 0.28 +/- 0.07, MK 421-group (N = 9) 0.03 +/- 0.01 ml/min. Renal blood flows were comparable in both treated groups. Only the left kidneys of rats treated with MK 421 showed a prominent tubular atrophy. Seven days after declipping of the left renal artery and right nephrectomy a considerable restitution of the tubular structure had occurred in the MK 421-group. The recovery of tubular epithelial cells was paralleled by a rise in glomerular filtration rate: MK 421 group (N = 7) 1.25 +/- 0.08 ml/min. Thus, the clipped kidney in two kidney, one clip hypertensive rats showed functional and morphological signs of impairment when systemic arterial pressure was reduced to the normal range. The alterations of the clipped kidney were most pronounced in rats with renin-angiotensin system-blockade.

The development of an age-dependent glomerulosclerosis and proteinuria was investigated in two strains of rats in a model of moderate hypertension comparing rats of the Milan Hypertensive Strain (MHS) with rats of the Milan Normotensive Strain (MNS). Serum creatinine, urinary protein excretion, renal morphology (light- and electronmicroscopy) and morphometry of the media thickness of the intrarenal arteries and of the thickness of the glomerular basement membrane were studied in 2- to 16-month-old MHS and MNS rats. Serum creatinine did not differ between MNS and MHS rats in any age group. MNS rats developed a significant proteinuria which coincided with a glomerulosclerosis in about 22% of the glomeruli at 13 to 16 months. In contrast, urinary protein excretion in MHS rats remained stable during the entire observation period; glomerulosclerosis occurred only in 3% of the glomeruli at 13 to 16 months. As a consequence of hypertension media thickness of intrarenal arteries of MHS rats significantly exceeded that of MNS rats, in the interlobular arteries already at 2 months and in the arcuate arteries at 13 to 16 months. In contrast, thickness of the glomerular basement membrane of MHS rats never exceeded that of MNS rats. From these data we conclude, that glomeruli of MHS rats may be protected against the development of an age-dependent glomerulosclerosis and proteinuria. Further support for this conclusion may also be derived from recent experiments showing that the tubuloglomerular feedback sensitivity is significantly higher in MHS than in MNS rats (41).

This paper sets out the arguments for drug treatment of chronic glomerulonephritides (GN). Although the pathogenesis and mechanism of progression of chronic GN remained to be clarified, on the basis of controlled studies performed to date, there is a strong case to be made for an aggressive treatment approach to this disease spectrum. For instance, in patients with idiopathic membranous glomerulonephritis a six months treatment with chlorambucil (0.2 mg/KG/day) or prednisone (0.6 mg/KG/day) each given once a day over a period of three months has recently been shown to improve the outcome of the renal functional parameters after three years follow up. In another controlled trial a daily dose of 225 mg dipyridamole and 975 mg aspirin given over 12 months in patients with membrano-proliferative GN type I has been reported to normalize the increased platelet consumption rate and to stabilize the glomerular filtration rate. A third trial has demonstrated that the combined use of cyclophosphamide (100 mg/day) and prednisone (30 mg/day) over several months was superior to the use of prednisone alone (40 mg/day) in improving the long-term prognosis of diffuse-proliferative lupus nephritis (type IV, WHO). In some entities, however, as in IgA-nephritis there is still no evidence for a specific treatment improving the course of the chronic glomerular disease. Other therapeutic problems have to be solved: thus, in patients with minimal change nephropathy with a steroid dependent nephrotic syndrome the benefit of cyclophosphamide (given over three months) or of cyclosporin A is still being investigated. Furthermore, there is some evidence that progression of chronic GN, particularly that of glomerular sclerosing, can be prevented by a low protein diet. The role of eicosanoides and their inhibitors in this context has not yet been fully investigated. The different drug trials and new therapeutic concepts indicate a rapid development of chronic GN treatment. Therefore, a failure to treat actively is difficult to understand.

Structural arterial adaptation and decompensation were studied in the contralateral untouched kidneys of two-kidney, one clip hypertensive rats 1 to 64 days after constricting one renal artery. Focal necroses of intrarenal arteries were observed as early as 24 hours after starting the experiment. The necroses reached their maximum on Day 8 and thereafter decreased significantly in spite of still increasing blood pressure values. After 8 days the media thickness of the interlobular arteries was significantly increased by more than 30% and remained so until the end of the experiment. Blood pressure levels as measured by tail plethysmography were nearly normal within the first 4 days. The continuous 24-hour blood pressure recording in the conscious rats, however, showed shortlasting intermittent hypertensive spikes as early as 6 hours after renal artery constriction. In spite of these acute hypertensive peaks, which frequently exceeded 200 mm Hg, intimal lesions, potentially leading to malignant nephrosclerosis, began to appear after only 2 weeks. Thus, the development of nonobliterating, acute focal necroses of intrarenal arteries in the earliest stage of two-kidney, one clip hypertension may be explained by intermittent hypertensive episodes accompanied by a segmental overstretching of the nonadapted vascular bed. On the other hand, the occurrence of obliterating malignant nephrosclerosis in the presence of severe hypertension may also depend on the previously changed composition of the vessel walls.

Bisher stehen fur eine Nierenprotektion fur langere Ischamiezeiten in situ zwei Verfahren zur Verfugung: a) die Oberflachenkuhlung mit Eis und b) die Perfusionskuhlung entweder mit Ringer-Laktat oder mit der Sacks-Losung.