Cure of Goodpasture's disease.

Goodpasture's Disease is an explosive multisystem disease presenting initially as a pulmonary-renal syndrome. There is often little margin for error in making an early correct diagnosis to avoid respiratory and renal failure. Complications of invasive diagnostic testing and aggressive immunosuppressive treatment often lead to other organ dysfunction due to infection, hemodynamic disturbances, fluid and electrolyte challenges, and nutritional deficiency. Artificial organ therapy is often needed for pulmonary and renal support, for immunomodulation, and for nutritional replacement. The outcome is often considered satisfactory if the patient survives the acute presentation. Persistent organ failure is quite often the case, especially renal failure. Quality of life is often improved if there is subsequent renal transplantation. By then the patient may be considered "cured". Two cases are described below, contrasting young and elderly white females both in previous good health who developed rapid onset of Goodpasture's disease. One was cured after transplantation, and one was cured without transplantation. The severity of the renal involvement was the same for both patients. Cure of Goodpasture's Disease in the native kidneys is uncommon; a review of the literature is provided.

Inter-organizational responses to AIDS: a case study of the Worcester AIDS Consortium.

This case study focuses on development and community coordination of AIDS-related services and on coalition building. Its subject is the Worcester (Massachusetts) AIDS Consortium. The objectives are to: (1) describe the environmental conditions and pre-existing networks which facilitated the formation of the Worcester AIDS Consortium; (2) articulate processes which occurred during the formative, organizational and operational phases of the Worcester AIDS Consortium's development; (3) explore social and community goals and Consortium activities; and (4) document Consortium accomplishments. Data were collected through key informant interviews and review of archival materials. Information about the Worcester AIDS Consortium experience is compared with concepts and principles suggested by organizational theories and frameworks.

Volume homeostasis in calves with artificial atria and ventricles.

We examined whether replacement of cardiac atria and ventricles with total artificial hearts (TAH), a procedure that removes cardiac nerves and all sources of atrial natriuretic factor (ANF), would cause alterations in volume homeostasis in awake calves. Preoperatively, extracted plasma immunoreactive (ir)ANF levels were 13.3 +/- 0.6 and remained postoperatively at 10.5 +/- 0.4 pg/ml (P less than 0.01). TAH implantation caused systemic and pulmonary hypertension (P less than 0.01), salt retention, edema, and significant elevations of plasma renin, aldosterone, and arginine vasopressin. In intact calves rapid infusion of 6 liters of normal saline raised irANF levels to 73.7 +/- 6.5 pg/ml (P less than 0.01) and elicited a large natriuresis and diuresis. No such response to 6 liters of normal saline was obtained after calves had recovered from TAH implantation. Reduction of cardiac output (CO) by 50% caused further salt retention and no change in irANF levels. Elevation of CO back to and 33% above base line produced only a diuresis, whereas salt retention persisted and irANF levels remained unchanged. The same maneuvers elicited in surgical control calves (artificial ventricles only, largely intact atria) a significant increase in irANF levels and a diuresis and natriuresis. In conclusion, alterations in volume homeostasis observed after TAH implantation seem to be the consequence of at least two pathophysiological mechanisms: 1) functional ANF "deficiency," characterized by apparently unregulated ANF secretion from noncardiac sites, and 2) cardiac denervation.

Atrial natriuretic factor and salt adaptation in the teleost fish Gila atraria.

It is unknown whether atrial natriuretic factor (ANF) is a mediator of environmental salt tolerance in euryhaline teleost fish. This was investigated in anesthetized Gila atraria, a euryhaline teleost native to springs of pleistocene Lake Bonneville. Plasma levels of immunoreactive (ir) ANF [using anti-human ANF-(99-126) antibodies] in fish obtained from a "fresh water" spring were significantly lower (146 +/- 27) than those in fish obtained from a "1% NaCl" spring (347 +/- 21 pg/ml, P less than 0.01). Electron micrographs of fish atrial and ventricular cardiocytes demonstrated many perinuclear granules, which closely resembled ANF-containing secretory granules seen in mammalian atriocytes. Fish heart extract contained ANF-like material of 3 kDa, which caused a marked diuresis and natriuresis in rats. In a second study, fish from a 1% NaCl spring were kept in tanks. One-third of the fish were maintained in 1% NaCl and one-third each were either adapted to fresh- or high-salt water. After 12 days, plasma irANF levels in 1% NaCl fish were 343 +/- 55, in fresh water fish 213 +/- 20 and in high-NaCl fish 691 +/- 79 pg/ml. These values differed significantly from each other (P less than 0.01). There was a close correlation between plasma irANF levels and both environmental and internal salt concentration. These data suggest that piscine ANF is an as yet unrecognized mediator of salt tolerance in this teleost and that ANF in these animals closely resembles mammalian ANF.

Renal tubular function in glycerol-induced acute renal failure.

The purpose of this study was to examine proximal and distal tubular function in rats with nonoliguric, myohemoglobinuric acute renal failure (ARF). ARF was induced with glycerol (50%, 10 ml/kg of body wt, i.m.), and renal function was studied 24 hours after glycerol or saline (controls) injection. Glycerol injection caused a 50 to 90% depression in GFR and a significant rise in blood urea nitrogen concentration. Animals with ARF exhibited glycosuria with normal blood sugar levels and a striking depression in tubular glucose reabsorption per milliliter of GFR. The capacity to reabsorb (mEq/liter GFR) was intact at normal blood bicarbonate levels, but was markedly depressed when blood bicarbonate was raised. The tubular maximum for para-aminohippurate (PAH) secretion and the renal extraction fraction of PAH were strikingly depressed in rats with ARF. Distal acidification as assessed by the urine-to-blood gradient of PCO2 (UB PCO2) was normal both during maximal alkalinization of the urine with bicarbonate (urine pH, approximately 7.8) or during neural phosphate infusion (urine pH, approximately 7.0). Net acid excretion per milliliter GFR and minimal urine pH (less than 5.5) following 3 days of ammonium chloride ingestion was similar in control and ARF animals. Potassium excretion was intact in maximal urinary osmolality were significantly altered in animals with ARF. Cortical and outer medullary Na-K-ATPase specific activities were significantly depressed in ARF rats. This occurred as a consequence of enzyme loss and not secondary to alterations in enzyme kinetics of absolute tubular sodium reabsorption. Light and electron microscopy showed diffuse proximal tubular damage, whereas glomeruli and distal tubules were intact. These data demonstrate that glycerol injection produces a diffuse proximal tubular transport defect associated with histologic and enzymatic alterations.