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A 28-year-old woman presented with dizziness and arterial hypertension. She reported a daily intake of 300 mg liquorice.Laboratory analysis revealed hypokalaemia of 2.5 mmol/l and an elevated serum renin activity of 18.6 µg/l/h. Abdominal ultrasound and magnetic resonance imaging showed a circumscribed non-homogenuous round lesion (18 × 22 mm) in the upper third of the right kidney. Selective catheterization of the renal veins revealed increased renin activity in blood from the right renal vein, suggestive of a renin-producing tumor.Initially antihypertensive therapy with the direct renin receptor antagonist aliskiren was started and followed by a partial nephrectomy, which brought about adequate blood pressure and potassium levels.The constellation of hypokalaemia and hypertension often leads to important causes of secondary hypertension such as primary hyperaldosteronism or renal artery stenosis. But less frequent causes should also be considered in the differential diagnoses, such as liquorice overindulgence or reninoma.

The renin angiotensin system is an important system for the regulation of blood pressure and salt and water homeostasis. As a pathogenetic factor it is involved in the development of several forms of renal hypertension and, furthermore, it participates in the pathogenesis of primary and secondary hypertension. The regulation of the activity of the system is under the control of neuronal and hormonal mechanisms and depends on blood pressure and plasma concentrations of sodium chloride. With the development of converting enzyme inhibitors and their vasodilator, diuretic and sympatholytic actions a new important antihypertensive principle for lowering blood pressure was found. In this context also local renin angiotensin systems which have been described for several tissues have to be discussed as a possible target of action for converting enzyme inhibitors.

The review discusses the pathophysiology of the renal mechanisms of blood-pressure control. The physiology of the renin-angiotensin system is described and the mineralo-corticoid function has also been considered. The implications of alterations of these systems in various nephropathies are briefly summarized (renal artery stenosis, infarction, Page's syndrome, acute glomerulonephritis, essential hypertension a.o.).

A 34-year-old woman developed uremia secondary to severe renal thrombotic microangiopathy after 3 years intake of oral contraceptives. In this particular case manifestation of end stage renal failure was preceded by an unusually long lasting period of nine months with benign hypertension. Even during the final stage (3-4 weeks) prior to complete development of uremia only once hemolysis but no malignant hypertension was observed. Only close long term follow up including renal biopsy and subtile functional tests may provide information whether and/or when hypertension due to oral contraceptives turns to become--at least in part--renal hypertension and also becomes persistent. This observation does not give evidence that benign hypertension causes renovascular damage and thus renal failure. Plasma renin activity was found to be basically elevated and furthermore stimulated e.g. by dialyses. However, this single observation does not permit any conclusion about a pathogenetic role of renin in creating hypertension by e.g. renal vasoconstriction or--despite hypertension--collapse of the capillary network.The case of a 34-year-old woman who developed uremia secondary to renal thrombotic microangiopathy after taking oral contraceptives for 3 years is reported. The case is unusual in that the clinical manifestations of nephropathy and terminal kidney failure were preceded by an almost 1-year development with benign hypertension. During the final stage (3-4 weeks prior to complete development of uremia), hemolysis was observed only once and malignant hypertension not at all. The question, if and when reversible hypertension due to oral contraceptives becomes persistent renal hypertension, can be answered only after long-term observations with careful documentation (renal biopsy and nephrologic functional diagnosis). This case suggests that benign hypertension does not cause renovascular damage and renal failure. Plasma renin activity was found to be basically elevated and, furthermore, stimulated by e.g., dialysis. However, this single case does not permit any conclusions about a pathogenetic role of renin in creating hypertension by e.g., renal vasoconstriction or despite hypertension - collapse of the capillary network.

The localization of aminopeptidase A (APA; E.C. 3.4.11.7) in the kidney cortex of the golden hamster was demonstrated by histochemical means (simultaneous azo coupling technique; alpha-L-Glu-MNA as substrate and HNF as coupling agent). APA was shown in the renal corpuscle (mainly podocytes and epithelium of the Bowman's capsule), the brush border of the proximal tubule, the perivascular tissue and some peritubular capillaries.--The demonstration of APA in the perivascular tissue of the juxtaglomerular apparatus (JGA) appears to have bearing on the regulation of angiotensin effects in the JGA for APA is an angiotensin degrading enzyme.

The area of contact between the macula densa and the terminal vascular components, the vas afferens, the vas efferens and the mesangium (Goormaghtigh cells) of five glomeruli of the rat has been determined morphometrically using serial sections. The surface, the filtration area, the volume and the total length of the capillaries of each glomeruli has been estimated, and these data have been correlated. There is evidence, that a contact between the macula densa and the mesangium always exists, a contact to the vas afferens is not obligatory.

A technique for SEM demonstration as well of the muscular architecture in the media of the blood vessels, as the granular juxtaglomerular cell complex in the wall of the afferent arterioles in the kidney is described. This method consists in an incomplete maceration and washing process in vascular cast preparations.

The case histories of 2 children with the typical characteristics of Bartter's syndrome are reported. The differential diagnosis from other forms of hypokalaemia, as well as pathophysiology and clinical manifestations of this syndrome are presented. The therapeutic effect of indomethacin, an inhibitor of prostaglandin synthesis, is discussed; side effects of this treatment are pointed out.

Author recommends for staining of the JGC-granula after oxydation with periodic acid a solution of phosphotungstic acid hematoxylin ripened by kalium iodate, and for counterstain an orange G solution.

Starting from the ultrastructural differences observed between the juxtaglomerular apparatus of the rat and that--only very rarely analysed--of the guinea pig kidney, the authors supposed that enzymhistochemical differences might also exist. This hypothesis could be confirmed by the results obtained in the Macula densa- and the Goormaghtigh-cells (Tab. 1 and 2). Indeed, in both places the Isocitrate dehydrogenase- and the Malate dehydrogenase-activities are stronger in the guinea pig than in the rat. On the other hand, the Glucose-6-phosphate and the 6-Phosphogluconate dehydrogenases show clearly weaker activities in the guinea pig Macula-cells compared with those of the rat, where these two enzymes give by far the strongest reaction. Metabolic differences might be related to the described diversities of the enzyme equipment.

A 38-year-old female patient developed a Pseudo-Bartter's-Syndrome with hypokalemic alkalosis, hyponatremia and hyperrenism as the result of the abuse of diuretics (furosemide, spironolactone, thiabutacide) for a period of more than 10 years. The needle biopsy specimen from the kidney showed a hyperplasia of the juxtaglomerular apparatus and of the mesangium cells as the morphologic basis of hyperrenism, a focal vacuolisation of the proximal tubular epithelium and a focal atrophy of the distal tubules. The pathogenesis of the tubular alterations and their possible relation to hypokalemia, hypoxemia or drug-toxicity is discussed, a satisfactory interpretation, however, cannot be given. The encroachment of proximal tubular epithelium on the parietal layer of Bowman's capsule is another striking pathoanatomical finding, and considered a compensatory mechanism under the continuous loss of water.

The adaptability of the kidney in heart-failure is restricted. This is due to a sympathetically mediated renal vasoconstriction, forming part of a sympathetically induced general rearrangement of haemodynamics. This is reflected in a rise of the total peripheral vascular resistance and of the right auricular pressure and can be normalized to a large extent by sympathetic gamma-blockade. The renal vasoconstriction reduces the glomerular filtration rate and, thus, the tubular sodium load. Simultaneously, possibly by the same sympathetic stimulus, more renin is liberated from the juxtaglomerular apparatus. This increases the production of angiotensin and in turn, raises the production of aldosterone. By the combined effect of the reduced glomerular sodium load and aldosterone-mediated increase in tubular reabsorption of sodium, sodium and water will be retained in the body. During the night-rest the load on the circulatory system diminishes. In the early stages of heart-failure this emergency circulatory reaction, therefore, subsides and the rise of the renal fraction of the cardiac output leads to the excretion of the retained fluid and is the basis of nocturia.

Quantitative data are presented on the glomeruli in the human, dog and rat kidney. Micropuncture techniques for the determination of filtration pressure and filtration rate are described. The final part of this paper deals with the dynamics of glomerular ultrafiltration. The roles are discussed of filtration equilibrium/disequilibrium and of the renin-angiotensin systems in the filtration process.

Kidney biopsy specimens of three patients with a special form of hypoplasia, the oligomeganephronic hypoplasia (Oligomeganephronie) were studied with light- and electron-microscopy as well as morphometric methods. The morphometric measurements demonstrated that there were no quantitative differences of the glomerular components between normal and oligomeganephronic glomeruli of patients of the same age. All of the structures measured--glomerular capillary surface, glomerular volume, volume of the glomerular capillary lumina and volume of Bowman's capsular space--were increased about 5.4 times. The volume of the proximal and distal tubules per mum tubular length in oligomeganephronic patients was disproportionally increased. The total number of glomeruli was more diminuished than mentionned in the literature until this time. The secondary glomerular sclerosis, initially focal, was progressive and supposed to be caused by "chronic overwork".