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Biomedical subjects

W C Waltzer

Publications and source records attributed to W C Waltzer.

At least 73 records · Page 4Linked to original sources

Etiology and pathogenesis of hypertension following renal transplantation.

Hypertension is a common feature of end-stage renal disease (ESRD) and constitutes a major risk factor for accelerated cardiovascular disease and premature death. While a reduction in the incidence and severity of hypertension is one potential benefit of kidney transplantation, hypertension often remains as a problem after transplantation, even in recipients of wellfunctioning allografts. Despite many studies of the underlying etiologic factors, the mechanisms implicated in post-transplant hypertension are still incompletely understood. A number of variables, including status of the diseased native kidneys, steriod therapy, rejection, recurrence of original disease, activation of the renin-angiotensin system, sodium and calcium metabolism, and transplant renal artery stenosis may play a role in the etiology of hypertension after transplantation. Patients with persistent high blood pressure for more than 3 months after transplantation should be thoroughly investigated, with controlled sodium intake so that proper medical or surgical therapy can be implemented. Since sodium restriction, radionuclide renal scanning, renin levels, or responses to saralasin or captopril may not provide a clear index of various possibilities, an accurate differential diagnosis my also require invasive procedures such as arteriography and/or renal biopsy.

Blood Pressure↗

Cortex perfusion index: a sensitive detector of acute rejection crisis in transplanted kidneys.

Damage to the renal cortical microcirculation, an early event in the course of acute rejection crisis (ARC), usually precedes measurable functional derangements in the transplanted kidney. Direct assessment of cortical blood flow by radionuclide renography may provide a sensitive and reliable index to the diagnosis of ARC, with particular regard to the differential diagnosis of ARC and ATN. Computer generated time-activity curves of global, cortical, and medullary renal blood flow were analyzed in 67 instances (35 patients) of renal allograft dysfunction and correlated with needle biopsy of these kidneys. No increase in cortex perfusion index (CPI), i.e., decrease in cortical perfusion, was found when the patients were suffering from ureteral obstruction or drug and viral nephropathy (mean perfusion index (PI) increase (8%). In contrast, a marked increase in CPI of 193% was noted in ARC. Global and medullary PI increased only 116%. As a result, global and medullary PI were capable of diagnosing ARC in only 73% and 55% of the cases, respectively, whereby cortex PI correctly diagnosed ARC in 94% of the cases. Selective analysis of cortical perfusion may thus enhance the accuracy of [99mTc]DTPA scans (radionuclide renograph) for the early detection of ARC and in differentiating ARC from nonimmunological causes of kidney allograft dysfunction.

Graft Rejection↗

Immunological consequence of renal transplantation and immunosuppression. I. Alterations in human natural killer-cell activity.

The role and activity of natural killer (NK) cells following renal transplantation remain unknown. To monitor NK activity, a 51Cr release of K-562 targets in prednisone- and azathioprine-treated patients receiving renal allografts was utilized. In 18 patients in whom NK activity was measured prior to and after transplantation, a significant diminution in NK activity within 3 weeks following transplantation was demonstrated compared to pretransplant values (34.71 vs 12.20%, respectively; P less than 0.001). In 11 subjects who had NK activity assayed at various intervals after transplantation but not prior to allografting, mean NK values were markedly lower (mean, 14.2%) than those of normal volunteers or patients maintained on hemodialysis (P less than 0.001). The latter two control groups demonstrated no difference (P = NS) in mean NK activity (39.46 vs 35.82%, respectively). In 5 of the 29 patients evaluated with good long-term graft function (mean, 2.7 years), restitution of normal NK activity was demonstrated. In two patients with bacterial infections, NK activity increased from 39.29 to 51.7% and from 13.54 to 20.00%. After infection, these values were 35.3% in the former and 3.39% in the latter. Viral infection did not appear to affect NK activity significantly. NK activity was increased in only one of seven patients with documented rejection episodes. In three of such patients, NK activity declined significantly following pulse methylprednisolone therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Retroperitoneal haemorrhage with abscess formation complicating Waldenström's macroglobulinaemia.

The complications of bleeding in patients with Waldenström's macroglobulinaemia (WM) are relatively well described. The pathophysiology of such a haemorrhagic diathesis is complex and involves the inhibition and depression of coagulation factors as well as qualitative and quantitative platelet abnormalities. Treatment of WM must be targeted at the underlying lymphocellular malignancy, but amelioration of the hyperviscous state and component transfusion(s) to correct abnormal coagulation parameters will decrease the incidence of bleeding. A case of WM with E. coli urinary tract infection and subsequent retroperitoneal haemorrhage with abscess formation and sepsis is presented. The pathophysiology and management of such patients is described.

Abscess↗