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The patient described in this clinical demonstration suffered from severe myasthenia gravis shortly before the detection and for 3 years after surgical removal of a cystic thymoma. At the end of this period, when the myasthenia subsided, she developed systemic lupus erythematosus simultaneously with pleural implantation metastases of the thymoma. After local radiation therapy and under systemic immunosuppression she has remained asymptomatic since the spring of 1978. The pathogenetic and immunogenetic basis of myasthenia gravis and autoimmune diseases associated with thymoma and thymus hyperplasia is reviewed, and a plea is entered for more comprehensive and integrative internal medicine.

In a 20 months' period 20 patients were dialyzed at the Cantonal Hospital, Lucerne, because of acute renal failure (ARF). Contrary to expectation, the main cause was not circulatory failure but traumatic and nontraumatic rhabdomyolysis (5 patients), septicemia (9 patients) and endogenous and exogenous intoxications. In only 2 patients did shock seem an important factor in the pathogenesis of ARF. In view of the many causes of rhabdomyolysis, the frequency of patients with myoglobinuric ARF is hardly surprising. Case history, brown-colored urine with a positive reaction for hemoglobin in the absence of significant hematuria and without significant hemolysis (as judged by the color of the plasma or serum) and, most important, high creatine kinase (10(4) to 10(6) U/l) point to the correct diagnosis. In patients who had undergone trauma or surgery the main cause of ARF was uncontrollable infection. A long interval between the accident or operation and the onset of ARF was typical in these cases. Both hemodialysis and peritoneal dialysis are adequate methods of treatment for ARF. For technical reasons, however, in more than 50% of patients with ARF due to trauma or surgery, peritoneal dialysis is not feasible. On the other hand, in patients with cardiovascular instability continuous arterio-venous hemofiltration serves as an alternative to hemodialysis. With the introduction of Y-shaped dialysis catheters and the single needle system with double pump and controlled ultrafiltration, hemodialysis has become an easier and safer procedure. For patients with prolonged-course ARF the authors prefer a combination of initial hemodialysis, followed by peritoneal dialysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Osteolytic lesions of bone in multiple myeloma may be treated by florides. A patient is reported who had IgA-Myeloma, was treated with high doses of sodium floride for 16 months and developed the clinical and radiological picture of advanced fluorosis. Within one year after discontinuing sodium fluoride therapy the soft tissue calcifications disappeared almost completely. High bone turnover may account for the accelerated deveopment and disappearance of fluorosis in myeloma. Progressive renal failure due to myeloma and, perhaps, increased susceptibility of destructed bone to fluorides advocate restricted use of fluorides in the treatment of osteolytic bone lesions in myeloma.

The question of what factors determine the significance of abnormal electrolyte findings is discussed with reference to a number of examples of acute electrolyte emergencies (hyponatremia, hypernatremia, hypokalemia, hyperkalemia, metabolic alkalosis). In addition to the extent of the deviation from normal and the clinical manifestations already present in all cases, it is principally the rate of dysfunction which determines the action of a clinical or laboratory-determined electrolyte deviation.

The case is presented of a young woman with partial lipodystrophy and intramembranous glomerulonephritis. Light and electron microscopic changes in the kidney biopsy are described and discussed. With immunosuppressive therapy very slow progression of the renal insufficiency was observed. Finally, regular dialysis treatment was required to sustain life. The follow-up after detection of intramembranous glomerulonephritis lasted 8 years.

Observation of a patient who developed serious hypernatremia during peritoneal dialysis with a dialysis fluid containing 135 mval Na+/1 prompted investigation of net water, sodium, potassium and chloride transport during 45 peritoneal fluid exchanges with standard dialysis solutions containing 1.5 and 4.5 g% glucose. With both solutions and an equilibration time of 0 min, net ultrafiltration was observed (89 ml and 230 ml per exchange respectively). In both groups the calculated sodium concentration of the ultrafiltrate was considerably lower than plasma sodium concentrations (27.0 mval/1 and 36.9 mval/1 respectively, resulting in a new sieving coefficient of 0.20 and 0.27 respectively. Therefore, the free water deficit resulting from peritoneal ultrafiltration is directly responsible for the hypernatremia observed during peritoneal dislysis. While the potassium and chloride transport observed in these studies can be explained by diffusion processes along a given concentration gradient, sodium transport and sodium concentrations raise the question of more complex mechanisms. The data are discussed with reference to the relative significance of diffusion processes versus bulk flow and solvent drag.

In 8 ambulatory patients with stable essential hypertension (WHO grade I and II) the effects of a new beta-blocker with marked sympathomimetic activity on arterial blood pressure, creatinin clearance and renal plasma flow, as measured by total PAH clearance (constant infusion technique), were studied. In contrast to previous findings no significant reduction in creatinin clearance or renal blood flow was observed during a 3-5 weeks' observation period. The small reduction in calculated renal vascular resistance was not statistically significant. In addition to its postulated peripheral vasodilatory effect, bufuralol appears to interfere less than propranolol with renal hemodynamics and renal excretory function.

To continuously monitor the impact of autopsy results, a short questionnaire was forwarded with each list of autopsy diagnoses to the clinician who had requested the autopsy. This continuous feedback between clinician and pathologist reveals unsolved problems and provides the opportunity for their interdisciplinary evaluation. The 1188 autopsies were done from 1980 to 1984 at the Institute of Pathology for the Medical Clinic, Cantonal Hospital, Lucerne, an acute-care medical teaching hospital department containing about 200 beds. The autopsy rate was 52% for in-hospital deaths. The clinician deemed that about 9/10 of all autopsies had confirmed his diagnosis. About 3/4 of all autopsies disclosed previously unknown and clinically important findings. Major discrepancies between clinical diagnosis and autopsy findings were noted in about 10% of all autopsies. Further, in approximately 1/10 of all autopsies the findings were considered to be of potential therapeutic relevance had they been known before death. The results confirm the relevance of autopsy for the practice of controlled clinical medicine based on objective criteria.

A few years ago the kidney in chronic renal failure was described as a mass of tissue "without significance, vanishing into the disparity of thousands of fantastically altered organs of strange design and anomalous behaviour". In order to refute this opinion, some of the morphological and pathophysiological evidence is summarized which points to the fact that even in chronic renal failure the remaining nephrons that contribute to renal function behave as a rather homogeneous population characterized by appropriate adaptations of glomerular and tubular functions and by a persistent responsiveness to the changing needs of the patient.

In 15 patients with moderate to severe hypertension (WHO II--III) atenolol was evaluated against a thiazide diuretic (bendrofluazide) in a single blind crossover study. Systolic blood pressure values were lowered more efficiently by the diuretic, while diastolic pressure values were significantly better controlled by atenolol. Atenolol and bendrofluazide, by mere addition of the pressure effects of the single components, clearly afforded the best pressure control. Side effects of atenolol were frequent but mild, never causing major concern with the patients or a dropout from the study. Although the pressure response to atenolol was significantly better in the normal and high renin group of patients, there was no statistically significant correlation between the reduction in plasma renin and blood pressure induced by atenolol. In turn, the pressure response to the diuretic was significantly better in low renin than in normal and high renin patients.

A 32 year old female patient demonstrates the rare combination of a typical IgA nephritis and familial immunothrombocytopenia. Although this association may be purely fortuitous, our observation adds a new facet to a spectrum of reports on (familial) "thromborenal syndromes". The pathogenesis of the IgA nephritis has not yet been clarified. However, since IgA deposits are found relatively frequently in the mesangium in a number of diverse underlying diseases, there might be common etiological factors. In view of this possibility more attention should be directed to the investigation of IgA associated diseases.

Clinical experience with continuous ambulatory peritoneal dialysis (CAPD) is described in 12 patients. A survey over 8 months shows satisfactory results. Besides the numerous advantages of this treatment, peritonitis represents the main problem. Technical developments in the future will aim at a reduction of this risk.

A patient suffering from a metastasizing malignant melanoma of the skin developed diffuse melanosis of the skin and melanuria a few weeks before death occurred. At autopsy, disseminated metastases of malignant melanoma were associated with marked melanosis of the organs and particularly of the mononuclear phagocytic system. In addition, neutrophilic granulocytes of the peripheral blood frequently contained melanin granules. The presence of melanin in blood monocytes and granulocytes may be useful for the diagnosis of (metastasizing) malignant melanoma.

Microhematuria offers a wide spectrum of diagnostic possibilities. Once the finding is confirmed, the diagnosis of prerenal, renal-parenchymatous and postrenal (or even factitious) hematuria and differentiation between glomerular and nonglomerular bleeding sources is based on the patient's history, a complete clinical status, special urinary findings (mainly red cell casts, proteinuria and red cell morphology) and blood chemistry (serum creatinine or creatinine clearance). If on the basis of this information glomerular or renal-parenchymatous microhematuria seems likely, further diagnostic procedures include immunological tests and, if indicated and justified, renal biopsy. Urography and other imaging procedures, urinary cytology and cystoscopy (firmly indicated when doubts persist or all the evidence points to postrenal hematuria) are deferred whenever glomerular hematuria seems likely. The special aspects of isolated renal microhematuria are discussed.

Central pontine myelinolysis (CPM) occurred in a typical patient with severe alcoholism presenting with severe initial hyponatremia and a rapidly progressive pontomesencephalic syndrome. A review on 141 cases of CPM is presented and the ties between CPM, hyponatremia/hypoosmolality and the syndrome of inadequate secretion of ADH are discussed. Correct interpretation of the patient's history (alcoholism, severe wasting disease) and the clinical picture (initial hypoosmolality with acute or subacute pontomesencephalic syndrome, possibly locked-in syndrome) should permit correct in-vivo diagnosis more frequently than hitherto.

In uncharacteristic clinical symptomatology the excess of water or the water intoxication render themselves conspicuous less by the signs of an increased fluid content than by central-nervous disturbances. Among the results of laboratory examinations the hypoosmolarity measured cryoscopically always, the hyponatraemia in most cases prove the excess of free water. Exceptions are discussed. A decreased capacity of the elimination of water pathogenetically plays a larger role than primarily excessive water supply. Apart from acute and chronic renal insufficiency the various forms of the Schwartz-Bartter-syndrome (inadequate ADH-secretion) play an increasingly more important role. The therapy demands the reduction of every supply of free water, the treatment of the evoking cause and only in cases of exception the administration of hypertonic saline solution, at the most dialysis treatment.

After a female patient had presented with advanced renal failure, bilateral enormous increase in kidney size radiologically, urinary tract infection (E. coli) and septicemia, autopsy disclosed megalocytic interstitial nephritis (MIN). Clinical and pathological differentiation from renal parenchymal malakoplakia (RPM) is discussed. A literature survey of 15 cases of MIN and 35 observations of RPM points to certain differences between the two entities, i.e. an increased incidence of bilateral pathology in MIN, mor frequent extrarenal localizations in RPM, absent Michaelis-Gutmann bodies and a predominantly cortical distribution in MIN. The similarities, however, suggest that the two conditions might represent different stages of one and the same disease process.

On the basis of microsphere distribution, inert gas washout, and standard clearance data, the effects of acute hypoxia and hypercapnia on the kidney were studied in anesthetized, mechanically ventilated rats. Moderate hypoxia (mean PO2, 48 mm Hg) did not significantly change diuresis, GFR, and tubular sodium rejection. Due to a decrease in renal vascular resistance (R) from 40.1 to 31.8 mm Hg ml-1 min, mean renal blood flow stayed constant in spite of a significant drop in mean arterial blood pressure. Hypoxic changes in R were not accompanied by significant changes in intrarenal distribution of blood flow (IDBF). In severe hypoxia (PO2 less than 45 mm Hg) with oliguria and marked arterial hypotension, R was the lowest of all groups (28.8 mm Hg ml-1 min). Hypercapnia did not significantly change the renal excretory parameters, although an increase in R (without change in IDBF), together with a decrease in MAP caused a marked drop in mean renal blood flow. From these studies we conclude: 1) in the anestheized rat, acute hypoxia caused significant changes in intrarenal hemodynamics without changes in excretory function, 2) hypoxic renal vasodilation persists even in severe hypotension with oliguria and anuria, 3) in acute hypoxia and hypercapnia, changes in renal blood flow and renal vascular resistance are not accompanied by significant changes in IDBF.

The clinical and pathophysiological significance and epidemiology of magnesium and phosphorus excess and deficit are discussed. In daily routine both ions largely remain "the forgotten electrolytes". With both elements deficits are clinically more important than excesses. Dietary intake, gastrointestinal and renal losses, shifts between intra- and extracellular fluid and sequestration within the extracellular compartment are the essential factors which determine body stores and the extracellular concentration of the electrolyte. The clinical signs of excess and deficit often lack specificity and - in the case of phosphorus deficiency - involve almost any organ. Since treatment of deficits is easy and success is rapid and involves virtually no risk a timely diagnosis is all the more important but often requires a high index of suspicion.

Renal manifestations of sarcoidosis are rare. In addition to calcium nephropathy, granulomatous interstitial nephritis and glomerulo-nephritis (GN) account for most cases. The latter two manifestations are described in 4 patients and in a detailed review of the literature. In comparison to a nonselected population of sarcoidosis patients, granulomatous interstitial nephritis is found more frequently in male patients above 40 years of age; it is associated more frequently with other extrathoracic manifestations of sarcoidosis; and it causes renal insufficiency of varying degree, which is at least partially reversible with steroid therapy. Predominant findings are silent microhematuria, sterile pyuria, mild proteinuria and a variety of tubular functional disorders. Glomerulonephritis (39 observations) has been described with increasing frequency in sarcoidosis. Because of the well known immunological abnormalities of sarcoidosis, frequent association of sarcoidosis with GN could be expected but this association has not yet been proven statistically. Sarcoidosis-associated GN includes a variety of histological forms, viz. membranous, proliferative and sclerosing GN. Glomerulonephritis may appear before sarcoidosis. Conversely, both diseases may appear simultaneously, or GN may follow all other manifestations of sarcoidosis with a latency period of many years.

As indicated by changes in microsphere distribution in the rat, acute bilateral carotid artery occlusion (CAO) was found to cause a small but significant increase in outer cortical flow fraction. When renal perfusion pressure was kept constant, no redistribution occurred upon CAO. In denervated kidneys the redistribution induced by CAO did not differ from that observed in contralateral control kidneys. Animals pretreated with prostaglandin inhibitors showed a significant redistribution in the 'unprotected' right kidney and a minor increase in outer cortical flow fraction in the normotensive kidney. It is concluded that: (1) the increase in outer cortical flow fraction induced by CAO in the rat is due to an increase in perfusion pressure, and (2) that this redistribution is independent of sympathetic vasoconstrictor stimuli, catecholamines and prostaglandins.

By damaging cell membrane integrity, acute rhabdomyolysis leads to electrolyte shifts according to the concentration gradients and the liberation of intracellular substances. Diagnosis is confirmed by the presence of a high serum creatinkinase activity (CK) and myoglobinuria. For clinical purposes myoglobinuria is demonstrated by a blood-positive dipstick in the absence of hematuria or hemoglobinuria. Rhabdomyolysis is usually acquired and is rarely due to hereditary enzyme defects. The authors report on 61 patients admitted in the last 15 years with rhabodomyolysis. In the past 4 1/2 years the diagnosis was suggested by CK greater than 5000U/1 in 49 patients, representing 1.6% of all admissions in the departments of medicine and surgery. Originally described in crush situations, rhabdomyolysis has been observed with increasing frequency as a consequence of muscular stress and self crush due to coma or hemi- and paraplegia during the last decades. 24% of the patients with this diagnosis had had an intoxication, and in 70% there were multiple simultaneous causes. Autoimmune diseases, infections of bacterial, viral and fungal origin, endocrinopathies, and thermic and ischemic injuries can also provoke rhabdomyolysis. As a consequence of fluid shift into the damaged muscle a compartment syndrome may lead to vascular or neural defects. In 80% of cases there is initial hypocalcemia, turning later into hypercalcemia. Other frequent electrolyte disorders accompanying rhabdomyolysis are hyperkalemia, hyperphosphatemia and a widened anion gap. 6 of 13 patients showed the typical blood changes found in patients with disseminated intravascular coagulation. Acute renal failure developed in 30 patients, 15 of whom underwent dialysis or hemofiltration.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrolyte-induced situations which are dangerous to life usually result from disturbances of the extracellular volume (ECV), osmolarity, the potassium level or the acid-base equilibrium. In recent years (thanks to the wide spread use of hormone therapy for mammary carcinoma) severe hypercalcemia has increased in importance as a life-threatening complication, while hypocalcemia, at least in adults, should only very seldom lead to unexpected emergencies. As long as serious clinical symptoms do not suggest an emergency, assessment of the threat to the patient as a result of the existing electrolyte disturbance often causes some difficulty. Besides the extent of the deviation from normal, the rate of development of the disturbance determines the resulting danger: chronic hypo-osmolarity, and especially hyperosmolarity are occasionally tolerated without symptoms while acute disturbances of the same or a less extent lead to severe central nervous symptoms. A similar state of affairs is also true of the emergency situations arising from disturbances of the acid-base equilibrium, among which the respiratory disorders are particularly important clinically. In the case of threatening disorders of the potassium metabolism, the accompanying circumstances (digitalis, simultaneous disorders and treatment of the acid-base equilibrium) often determine the clinical significance and danger to the patient. Clinical symptoms, anticipation ("expecting the unexpected"), prevention and treatment of emergency situations of fluid volume, osmolarity, potassium and acid-base equilibrium are the subjects of this paper.