Traumatic renal artery thrombosis.

Traumatic bilateral renal artery thrombosis is a rare injury that may be under-diagnosed. The clinical hallmarks include epigastric or flank pain and proteinuria, or hematuria following blunt trauma to the back or abdomen. Traditional practice suggests that revascularization should not be attempted more than 20 hours after injury. A patient is described in whom the retroperitoneum was explored 48 hours after injury and was found to have bilateral renal artery thrombosis. Although no repair was attempted, renal function spontaneously improved over several weeks. The clinical course of this patient suggests that revascularization should be considered even if the diagnosis is made more than 20 hours after injury.

Time course of response to pulse methylprednisolone therapy in renal transplant recipients with acute allograft rejection.

All rejection episodes that occurred from 1990 to 1995 treated by the University of Colorado renal transplant service were evaluated through a review of patient charts. Seventy-one episodes of rejection were treated initially with pulse steroids consisting of pulse methylprednisolone, 500 mg/d for 3 days, with sufficient follow-up to determine whether the patient would respond to this treatment. There was no difference between responders and nonresponders to methylprednisolone treatment with respect to serum creatinine level at time of diagnosis, age of allograft, nadir serum creatinine level, or presence of oliguria. The time course of change in serum creatinine levels (in milligrams per deciliter) in responders and nonresponders was similar until day 5, at which time significant differences could be seen (P < 0.01). In the 34 patients treated with OKT3 (muromonab-CD3), statistically significant differences between responders and nonresponders were only seen at day 14, but the small number of nonresponders (n = 4) makes this analysis inconclusive. Based on these data, it appears one cannot truly evaluate whether a patient will respond to three daily pulses of methylprednisolone until at least 3 days have passed since completion of therapy.

Nephritic urinary sediment in embolic renal infarction.

Emboli to the renal arteries occurs most often in patients with underlying cardiac disease. Hematuria is a common feature of renal infarction, but the finding of erythrocyte casts in cases of renal infarction has not been commonly reported. We report a case of renal artery embolization in a patient who had transient nephritic urine sediment, and review the significance of this finding.

New classification with prognostic value in cirrhotic patients.

We evaluated a group of 21 cirrhotic patients with a standard 20 ml/kg water load. The patients segregated into three classes: class I (n = 6) had normal water load excretion, i.e. greater than 80% excretion over 5 h (mean 82.3 +/- 0.8%); class II (n = 8) had 20-80% excretion (mean 38.6 +/- 4.2%); and class III (n = 7) had less than 20% excretion (mean 12.9 +/- 1.2%). The patients in class III, who had profound impairment of water load excretion, were found to have a higher frequency of tense ascites, lower serum sodium concentrations, diuretic resistance, impairment of urinary sodium excretion, lower inulin and p-aminohippurate clearances, and elevations of plasma arginine vasopressin, aldosterone and norepinephrine concentrations. However, class III could only be distinguished from class II on the basis of excretion of a standard water load. No significant differences were found among the classes in liver function tests. We prospectively followed these patients. Classes I and II patients appear to have a good prognosis, if they avoid ethanol (4 of 5 patients still alive 42-56 months after evaluation). Class III patients have a poor prognosis independent of ethanol intake (all lived less than 5 months, except 1 patients who received a peritoneovenous shunt). Class I patients were found to tolerate continued ethanol consumption better than class II patients. Thus, an early intervention, such as the peritoneovenous shunt, may prolong survival among class III patients; however, this possibility needs to be evaluated in a larger prospective study.

P-31 nuclear magnetic resonance spectral changes in obstructed or dehydrated kidney.

Rat kidneys subjected to urinary obstruction or dehydration in vivo both develop marked increases in the area under a peak resonating in the phosphodiester region on their P-31 nuclear magnetic resonance spectra. The chemical species responsible for these changes were assessed using physiologic manipulations which altered the concentration of phosphate in the urine or increased the urine pH. Obstructed kidneys of rats fed a normal diet had a 140 +/- 50% increase in a peak resonating at 3.31 +/- 0.05 ppm after three hours of obstruction (P less than 0.01). Low phosphate diet which decreased urine phosphate concentration by 98% virtually eliminated this increase in peak area, where saline diuresis which decreased urine phosphate concentration by 50% markedly attenuated it. Acute phosphate loading which doubled urine phosphate concentration markedly accentuated the increase in peak area. Alkalinizing the urine with acetazolamide (changing urine pH from 6.2 +/- 0.2 to 8.0 +/- 0.1) shifted the resonance frequency of this increasing peak from 3.31 +/- 0.06 to 5.45 +/- 0.11 ppm (P less than 0.01). Rats fed a normal diet developed increases (57 +/- 15%, P less than 0.05) in a peak resonating at 2.84 +/- 0.03 ppm following 48 hours of dehydration. Rats fed a low phosphate diet had a comparable increase in the relative area of this peak (46 +/- 16%, P less than 0.05). Alkalinization of the urine did not affect the position or intensity of this peak under conditions of dehydration.(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonary embolus masquerading as pneumonia in a patient with Hodgkin's disease and nephrotic syndrome.

Fatal pulmonary embolus is an infrequent cause of death in patients with Hodgkin's disease who respond to initial therapy. This patient had associated minimal change disease and nephrotic syndrome that was responding to therapy, but had this complication. The diagnosis was delayed by the presentation that suggested pneumonia. A high index of suspicion for thrombotic complications and an aggressive diagnostic pursuit thereof are merited in these patients.

Atrial natriuretic factor (ANF) levels are elevated in rats bearing rejecting heart-lung allografts.

Intra-abdominal heart-lung grafts were transplanted into 8 rats across a major histocompatibility barrier. Four of the 8 rats were treated with Cyclosporin A (CsA) to prevent rejection. Atrial natriuretic factor (ANF) levels measured 6 days after transplantation revealed a significantly (p less than .005) higher mean ANF concentration in rats bearing a rejecting heart-lung allograft (642 +/- 148.0 pg/ml) compared to rats bearing a heart-lung allograft not undergoing rejection (200.8 +/- 13.07 pg/ml). ANF might be a useful noninvasive marker in the diagnosis of rejection in heart and heart-lung transplants.

Elevated plasma atrial natriuretic factor and vasopressin in high-altitude pulmonary edema.

A diagnosis of acute high-altitude pulmonary edema was made in five male skiers (age, 35.0 +/- 1.8 years) by history and physical examination and was confirmed by a characteristic chest radiogram showing alveolar infiltrates associated with a normal cardiac silhouette. Five healthy age- and sex-matched subjects with similar physical activity at the same altitude served as controls. Plasma sodium was 135.0 +/- 1.5 mmol/L in the acutely ill patients compared with 144.0 +/- 3.3 mmol/L in the controls (P less than 0.025). Mean plasma atrial natriuretic factor immunoreactivity averaged 17.6 +/- 5.6 pmol/L in patients with high-altitude pulmonary edema compared with 6.8 +/- 0.7 pmol/L in the controls at the same altitude (P less than 0.05). Elevated atrial natriuretic factor levels normalized to 7.5 +/- 1.9 pmol/L (P less than 0.05) during recovery in Denver (altitude, 1600 meters) 24 hours later. Plasma arginine vasopressin levels were 1.8 +/- 0.37 pmol/L in patients with high-altitude pulmonary edema at diagnosis compared with 0.92 +/- 0.28 pmol/L in controls (P = 0.07). The inappropriately elevated arginine vasopressin levels decreased to 1.29 +/- 0.37 pmol/L during recovery (P less than 0.025), but the lowered plasma sodium concentration had not normalized by discharge within 24-hours of transfer to Denver and averaged 135.8 +/- 1.2 mmol/L. The pathophysiologic implications of these findings are discussed.