Hepatitis C viral infection is associated with fibrillary glomerulonephritis and immunotactoid glomerulopathy.

The most common form of glomerular disease seen in association with hepatitis C virus (HCV) infection is membranoproliferative glomerulonephritis, with or without associated cryoglobulinemia. This study examines four cases of fibrillary glomerulonephritis and two cases of immunotactoid glomerulopathy in association with HCV infection. Findings at presentation included proteinuria, renal insufficiency, and hematuria. Renal biopsy revealed a membranoproliferative pattern of glomerular disease in five cases, and a membranous glomerulopathy with mesangial proliferative features in one. On immunofluorescence, all cases stained with IgG and C3. Electron microscopy revealed fibrils of the expected diameter, 16 to 28 nm in fibrillary glomerulonephritis and 33 to 45 nm in immunotactoid glomerulopathy. In only one case were cryoglobulins detected (at low titer and on only one of three assays). Antiviral therapy was not given in any of the six cases. Outcomes were mixed, with progression to renal failure occurring in two patients and persistent proteinuria with stable or improved renal function in three. Follow-up is not available on the sixth case. Both fibrillary glomerulonephritis and immunotactoid glomerulopathy have features that overlap with cryoglobulinemic glomerulonephritis. The relatedness of these three entities in a subset of patients with HCV infection suggests a common pathogenic mechanism of glomerular deposition of organized deposits.

Complications associated with central venous cannulation.

Some complications, such as pneumothorax, air embolism, and arterial laceration, may occur immediately after insertion. Others, such as infection, hydrothorax, phlebitis, and thrombosis, may occur later.

Sonographic pseudokidney after nephrectomy.

When interpreting renal sonograms, one should be aware of the possibility of mistaking fat and scarring in the renal fossa for a normal kidney in a patient with a history of prior nephrectomy. When in doubt, the ultrasound findings should be confirmed with a CT scan.

The kallikrein-kininogen-kinin system in patients with liver disease and ascites.

The urinary excretion of kininogen, kallikrein (total and active), and kinins were measured in 7 men with severe liver disease and ascites. The results were compared with a group of normal controls matched for sodium excretion. Significant reductions in kinin excretion were noted in the patients with liver disease which could not be accounted for by differences in age, plasma renin, aldosterone excretion or sodium excretion. Both active kallikrein and kininogen excretion were reduced suggesting that deficiencies of enzyme and substrate contributed to the kinin deficiency. The importance of kininogen in the physiologic regulation of kinin excretion in this clinical state is discussed.

Effects of changing salt and water balance on renal kallikrein, kininogen and kinin.

The kallikrein-kininogen-kinin system (KKK) has been implicated in the renal sodium excretion response to changes in dietary sodium. However, both increases and decreases in the activity of this system have been observed when urinary sodium excretion is augmented by a variety of maneuvers. To further evaluate the potential physiologic role of this system, we measured three components of the KKK system in urine. Total kallikrein, intact kininogen, and kinin were measured twice in normal individuals during balance on both a high (250 mEq/day) or low (10 mEq/day) sodium intake. A consistent and significant reduction in the activity of all three components of the KKK system was noted during the high salt intake. Furthermore, during the high sodium intake, further acute reductions in components of this system were observed when an acute saline but not water load was administered. The consistent response of the various components of the KKK system to both acute and chronic sodium loading suggests that the system is physiologically linked to the regulation of sodium balance. However, the directional changes argue against a primary natriuretic effect of this system.

Urinary kininogen: a possible regulator of kinin formation in normal individuals and subjects with essential hypertension, end-stage renal and liver disease.

Most previous studies have not significantly correlated urinary kallikrein to urinary kinins. We investigated whether urinary kininogen might influence kinin formation within the urine. On an ad-lib diet the 24 hour excretion of total and intact kininogen, kinins and kallikrein was determined in 24 control subjects, 20 untreated essential hypertensives, 12 with end-stage renal disease and 8 subjects with liver disease. Kallikrein and kinins were measured by a direct radioimmunoassay. Total kininogen was determined from the sum of preformed kinins and kinins generated after trypsin (intact kininogen). Cross reactivity between purified human low molecular weight kininogen and bradykinin antiserum was 3%. Total and intact kininogen were significantly correlated with kinins in controls, essential hypertension and liver disease. In essential hypertension, end-stage renal and liver diseases kinins were significantly decreased. This was associated with a reduction in kininogen but not kallikrein in essential hypertension and liver disease, and a reduction in kallikrein but not kininogen in end-stage renal disease. Thus, renal kinin generation in various states may be affected by either or both kininogen and kallikrein.

The role of urinary kininogen in the regulation of kinin generation.

The kallikrein-kininogen-kinin system has been postulated to play a role in the regulation of blood pressure and modulation of renal salt and water transport. The activity of this system has usually been determined by measurements of urinary kallikrein excretion. However, urinary kallikrein rarely correlates with simultaneously measured urinary kinins. To further evaluate the factors influencing urinary kinin excretion, we evaluated the role of urinary kininogen in this system. Urines were analyzed from normal subjects and individuals with untreated essential hypertension and end-stage renal disease. Intact urinary kininogen was significantly correlated with urinary kinins in normal subjects (r = 0.65, P = 0.003) and essential hypertensives (r = 0.52, P = 0.026). In both essential hypertension and end-stage renal disease, urinary kinins were significantly decreased (8.00 +/- 1.93, 0.90 +/- 0.18, P less than 0.05, respectively) compared to controls (23.73 +/- 5.20). In essential hypertensives, the reduction in urinary kinins was paralleled by a reduction in intact kininogen with a normal excretion of kallikrein. In end-stage renal disease, the reduction in kinins was paralleled by a reduction in kallikrein with a normal excretion of intact kininogen. This data suggests that kininogen may be an important determinant of urinary kinin excretion in various disease states.

Pathologic involvement of the urinary bladder in progressive systemic sclerosis.

We describe 2 patients with progressive systemic sclerosis (PSS) who manifested characteristic pathologic abnormalities in the urinary bladder. Increased connective tissue deposition in the lamina propria and between smooth muscle bundles was demonstrated in both patients and endovascular proliferation in small arteries of the bladder was noted in one patient. Both patients had persistent unexplained microscopic hematuria; one patient manifested urinary frequency and incontinence. The relationship of these clinical abnormalities to the pathologic findings in the bladder is unclear. Structural or functional abnormalities of the urinary bladder may develop in patients with PSS.

Elevated nicotine levels in patients undergoing hemodialysis. A role in cardiovascular mortality and morbidity?

The incidence of cardiovascular disease in patients with end-stage renal disease undergoing long-term maintenance hemodialysis is excessively high. The reason for this excess morbidity and mortality has remained unclear. Cigarette smoking is one factor that has been associated with increased cardiovascular risk. To learn more about the effects of tobacco smoking in these patients, nicotine levels were assayed in the serum of 10 patients with end-stage renal disease undergoing maintenance hemodialysis. Specimens were obtained before and after smoking one cigarette and following dialysis or an equivalent period in control subjects. Serum nicotine levels (+/-SEM) in control subjects measured 19.0 +/- 7.2 ng/ml initially, 36.1 +/- 8.2 ng/ml after smoking, and 9.3 +/- 3.5 ng/ml after a period of 4.35 hours. These compare with respective values of 76.6 +/- 16.8 ng/ml (p less than 0.004), 132.9 +/- 19.7 ng/ml (p less than 0.001), and 51.9 +/- 10.5 ng/ml (p less than 0.001) in patients undergoing hemodialysis. These data demonstrate markedly higher nicotine levels in hemodialysis patients compared with control subjects, which may have serious implications regarding morbidity and mortality.

Thallium-201 myocardial imaging in patients on chronic hemodialysis.

10 long-term hemodialysis patients had immediate and redistribution thallium-201 myocardial imaging performed after a course of hemodialysis. Subjects had EKGs done on the same day before and after dialysis. 3 of the 10 subjects had resting thallium-201 myocardial imaging obtained on non-dialysis days. 60% of the electrocardiograms showed changes with dialysis. All 13 thallium studies were abnormal, showing multiple transient filling defects at rest. Most subjects had permanent filling defects as well. It is concluded that hemodialysis patients have a high frequency of abnormal thallium-201 myocardial images at rest. The cause of these abnormal studies is uncertain.

Leiomyosarcoma arising in an arteriovenous fistula.

The case of a man who developed a leiomyosarcoma in association with a surgically created arteriovenous fistula is reported. This unusual complication of a dialysis fistula is the first reported case of a leiomyosarcoma occurring in a surgically created fistula.

Treatment of schistosome-induced glomerulonephritis. A case report and review of the literature.

A patient with membranoproliferative glomerulonephritis and renal dysfunction caused by Schistosoma mansoni was treated with oxamniquine. High levels of circulating immuno-complexes returned to normal following treatment, although renal function for the long term was unchanged. Specific antischistosomal therapy may be of partial benefit to patients with this disease.

Phantom urinary symptoms in hemodialysis patients.

Phantom urinary symptoms were reported by 12 or 24 hemodialysis patients surveyed. The symptoms were present in all age groups. The absence of any correlation between the occurrence of these symptoms and length of time and dialysis suggest that urinary phantoms in hemodialysis patients may persist over time in contrast to the gradual disappearance of phantoms symptoms resulting from amputation. No correlation was found between occurrence of phantom symptoms and sexual impairment, actual voiding of urine or symptoms of peripheral neuropathy.

The significance of beta-2 microglobulinuria associated with gentamicin therapy.

Gentamicin is a nephrotoxic agent known to damage the proximal tubule,--a site of low molecular weight (LMW) protein reabsorption and catabolism. The effect of gentamicin was investigated on three LMW proteins--amylase, light chains, and beta 2 microglobulin--and the effects were correlated on the latter to renal function as determined by creatinine clearance (GFR). The renal excretion of beta 2 microglobulin (beta 2M) was studied in 18 patients receiving gentamicin and eight control patients. Both gentamicin and control patients had similar mean ages and serum beta 2M. Twelve of the 18 gentamicin treated patients had marked increases in beta 2M excretion. The mean daily 2 beta microglobulin excretion for the gentamicin treated group was 10,511 microgram while that of the control group was 102 microgram. Serial determinations in 10 of the gentamicin treated patients revealed an increase in beta 2M excretion within 48 hours of starting therapy. No deterioration of GFR was seen in any patient. In four patients, beta 2M excretion decreased while still receiving gentamicin. The renal handling of amylase was found to be normal in four patients and mildly abnormal in three patients receiving gentamicin who also had increased beta 2M excretion. Urinary light chains were determined in four of these seven patients and found to be normal. It is concluded that gentamicin induces an early and often transient tubular proteinuria. This tubular proteinuria is not associated with clinical nephrotoxicity.

Electrocardiographic changes following dialysis.

We investigated electrocardiographic changes occurring after hemodialysis in 20 male patients with chronic renal failure. Changes in the configuration of T wave, ST segment and R wave consistent with ischemia were found in 30, 45, and 75%, respectively. Contrary to prior speculation the R wave height did not vary with the volume changes of body fluid occurring in dialysis. It is concluded that ischemic-appearing changes of uncertain significance are common in the postdialysis population.

Hemodialysis and pregnancy.

When severe renal failure requiring hemodialysis complicates pregnancy, there is hesitation to continue the pregnancy. However, successful hemodialysis in pregnancy is being reported with growing frequency. Fetal survival and even conception is possible in patients undergoing dialysis.

Polycystic kidneys without radiologic enlargement.

Polycystic kidneys in adults usually appear in the middle years and are described as large kidneys with most of their parenchyma displaced by a large number of cysts. Often the diagnosis is excluded if the intravenous pyelogram reveals kidneys of normal size. This report describes a patient with normal sized polycystic kidneys discovered at an advanced age.