Resolution of proteinuria secondary to bilateral renal vein thrombosis after treatment with systemic thrombolytic therapy.

A case of significant proteinuria occurred as a result of bilateral renal vein thrombosis secondary to dehydration, which resolved after treatment with urokinase. The patient developed nausea and vomiting from viral gastroenteritis with subsequent volume contraction. He later noted the onset of aching lower abdominal and flank pain. On admission, he was noted to have a serum creatinine of 1.7 mg/dL, and 4+ proteinuria on urinalysis. A 24-hour urine collection showed 2.34 g protein. A renal venogram showed bilateral renal vein thrombosis (RVT) without involvement of the inferior vena cava. Therapy was initiated with heparin at 1,000 U/hr, followed by intravenous (IV) urokinase, 4,400 U/kg bolus, followed by 4,400 U/kg/hr with continuous infusion for 12 hours. A repeat renal venogram done at this time showed partial resolution of thrombosis bilaterally. A second 12-hour infusion of urokinase at 5,000 U/kg/hr was performed; at this time, the patient reported resolution of his flank and abdominal pain. A repeat 24-hour urine collection showed 60 mg protein with a normal creatinine clearance. Levels of antithrombin III, protein C, and protein S were all normal. A renal biopsy was performed and showed normal histology on light, immunofluorescent, and electron microscopic evaluation. The patient has done well on no therapy and has had no recurrence of thrombosis or proteinuria after 2.5 years. This is a US government work. There are no restrictions on its use.

Sources of urinary catecholamines in renal denervated transplant recipients.

When a human kidney is transplanted, sympathetic nerves to that kidney are cut. We infused 3H-noradrenaline and then measured noradrenaline, dopamine and 3H-noradrenaline levels in the plasma and urine of renal transplant recipients and uninephrectomized control subjects. Less than 10% of 3H-noradrenaline cleared from the plasma appeared in the urine. Noradrenaline and dopamine appeared in the urine of transplant recipients at one-third the rate of control subjects, even though 3H-noradrenaline levels were slightly higher in the urine of transplant recipients. Transplant patients had a noradrenaline clearance of 128 +/- 50 ml/min, compatible with simple glomerular filtration, while controls had a higher calculated clearance of 229 +/- 41 ml/min. Plasma dopamine levels were very low compared with urinary dopamine. These results suggest that two-thirds of renal noradrenaline and dopamine depend on the presence of renal nerves. Almost all urinary dopamine comes from the kidney. For noradrenaline, urinary excretion is a very minor pathway for clearance from the plasma.

Catecholamine and thyroid hormones in traumatic injury.

During hyperthyroidism, hypothyroidism, and severe stress there is often an inverse relationship between plasma norepinephrine (NE) and thyroid hormones. We evaluated this relationship in patients who were severely burned, patients who had injury to both brain and body, patients with head injury, and patients receiving high dose barbiturates for head injury. Head-injured patients had a low thyroxine (T4), low triiodothyronine (T3), and high reverse T3. Phenytoin for control of seizures lowered T3 and T4 and increased thyroid-stimulating hormone. Burned patients had a strong negative correlation between NE and T3 (r = -.88, p less than .001). Patients with injury to both brain and body had a weak negative correlation between NE and T3 (r = -.5, p = .06). Patients with head injury showed no correlation between NE and T3. Severely injured patients had a close inverse relationship between elevated NE levels and depressed T3 levels. This relationship appears to depend on an intact CNS, as the relationship was disrupted by head injury and barbiturates.

Atrial natriuretic factor in renal failure and posthemodialytic postural hypotension.

Atrial natriuretic factor (ANF) levels were ten times normal in hemodialysis patients before dialysis. ANF was not cleared by the dialyzer membrane but plasma levels decreased 47% by the end of dialysis. Patients undergoing peritoneal dialysis had plasma ANF levels four times normal and had detectable ANF in their dialysate. Hemodialysis patients with a marked fall in BP after dialysis had higher ANF levels (P less than 0.05) and lower norepinephrine (NE) levels (P less than 0.05) associated with a failure to increase NE in response to dialysis. Elevated ANF levels are associated with postdialysis hypotension in hemodialysis patients.