Biomedical subjects

V E Torres

Publications and source records attributed to V E Torres.

At least 73 records · Page 4Linked to original sources

PubMed1992

Cyst fluid from human autosomal dominant polycystic kidneys promotes cyst formation and expansion by renal epithelial cells in vitro.

Autosomal dominant polycystic kidney disease (ADPKD) is characterized by progressive renal enlargement, culminating in renal insufficiency in over one half of affected individuals. The highly variable onset and clinical course of ADPKD may be due to factors extrinsic to the genetically defined renal cysts. In this study, cyst fluid samples from 12 nonazotemic and 18 azotemic ADPKD subjects were examined for in vitro biologic activity that promotes cellular proliferation and the secretion of fluid by renal epithelial monolayers, two pathogenetic mechanisms that have critical roles in the formation and the rate of expansion of renal cysts. Cyst fluid added to culture medium (final concentrations, 1 to 20%) caused Madin-Darby canine kidney cells and human kidney cortex (HKC) cells derived from primary cultures to form cysts in Type I collagen matrix. Cyst fluid stimulated the net transepithelial secretion of fluid by polarized monolayers composed of these same cells. Absolute levels of fluid secretory activity determined by MDCK bioassay were correlated directly with the rate of fluid secretion by HKC cell monolayers and with the extent of cyst formation by MDCK and HKC cells embedded in collagen matrix. The secretory activity of urine was negligible; secretory activity was detectable in the serum of normal and ADPKD subjects, but the levels were much lower than in cyst fluid. cAMP agonists prostaglandins E1 and E2, arginine vasopressin, and 8-Br-cAMP stimulated fluid secretion by MDCK and HKC monolayers, but these substances did not cause HKC cells to form cysts in collagen matrix, whereas cyst fluid did. Among other naturally occurring growth factors and autacoids, only epidermal growth factor and transforming growth factor alpha stimulated cyst formation by HKC cells; however, the capacity of cyst fluid to stimulate fluid secretion was not affected by treatment with antiserum to epidermal growth factor. It was concluded that potent, and possibly unique, substances in the cyst fluids of individuals with ADPKD support and augment biologic processes in renal epithelial cells that may be important in the promotion of progressive cyst expansion.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1991

Effect of inhibition of converting enzyme on renal hemodynamics and sodium management in polycystic kidney disease.

We compared the tubular transport of sodium and the erythrocyte sodium-lithium countertransport activity in hypertensive patients with autosomal dominant polycystic kidney disease (ADPKD) and in normotensive control subjects. In addition, we assessed the effects of inhibition of converting enzyme on renal hemodynamics and sodium excretion in hypertensive patients with ADPKD to provide information on mechanisms responsible for the increased renal vascular resistance and filtration fraction and the adjustment of the pressure-natriuresis relationship during saline expansion, observed in patients with ADPKD, hypertension, and preserved renal function. In comparison with normotensive control subjects, the hypertensive patients with ADPKD had lower renal plasma flows, higher renal vascular resistances and filtration fractions, and similar proximal and distal fractional reabsorptions of sodium. The administration of enalapril resulted in significant increases in the renal plasma flow and significant reductions in mean arterial pressure, renal vascular resistance, and filtration fraction, but the glomerular filtration rate remained unchanged. Despite the significant reduction in mean arterial pressure during inhibition of converting enzyme, the distal fractional reabsorption of sodium decreased while the total fractional excretion of sodium remained unchanged or increased slightly. No significant differences were detected between the normotensive control subjects and the hypertensive patients with ADPKD in erythrocyte sodium-lithium countertransport activity, plasma renin activity, plasma aldosterone concentration, or atrial natriuretic factor. These results suggest that the renal renin-angiotensin system plays a central role in the alterations in renal hemodynamics and sodium management associated with the development of hypertension in ADPKD.

Adult↗

PubMed1991

Oxalate, silicon and vanadium in acquired cystic kidney disease.

We have investigated the importance of several clinical and laboratory parameters on the development of acquired cystic kidney disease (ACKD) as detected by ultrasonography in 19 patients who had received dialysis therapy for at least three years. We were particularly interested on the possible effect of the serum levels of oxalate and silicon, which can produce tubular obstruction, and that of vanadium, which can affect cell proliferation. The severity of ACKD increased with the duration of dialysis and was greater in men than in women. Positive correlations were observed between the grades of ACKD and the levels of hemoglobin, hematocrit, and parathyroid hormone, while there was a negative correlation between ACKD and serum ferritin levels. The serum levels of oxalate, silicon, and vanadium, pre- and postdialysis, were markedly and significantly higher than those in normal controls, but there was no significant correlation between these levels and the duration of dialysis therapy or severity of ACKD. The pre- and postdialysis levels of vanadium were not significantly different, while the levels of oxalate and silicon were significantly lower in the postdialysis samples. No significant correlations were detected between ACKD and age of the patients, blood pressure, protein catabolic rate, efficiency of dialysis index, or the serum levels of iron, sodium, potassium, calcium, phosphorus, aluminum, and beta 2-microglobulin.

Dialysis Solutions↗

PubMed1990

Association of hypokalemia, aldosteronism, and renal cysts.

The recognition of renal cysts in two patients with chronic hypokalemia and the renal effects of hypokalemia in certain species of animals prompted this study of the possible association of hypokalemia and renal cysts in patients with primary aldosteronism or primary renal potassium wasting. Using CT scans, we studied 55 patients with primary aldosteronism, of whom 24 had cysts (44 percent). The cysts were more frequent in patients with adrenal tumors than in those with idiopathic adrenal hyperplasia. Sixteen of the 26 patients with tumors (62 percent) had renal cysts, which were often multiple and located in the medulla. Lower plasma potassium levels and higher serum aldosterone levels, urinary aldosterone excretion, and plasma renin activity were correlated with the extent of the cystic disease. Sequential observations indicated that prolonged hypokalemia can be accompanied by the development of renal scarring and that the size and number of cysts can decrease markedly in some patients after the removal of an adrenal adenoma. The association of hypokalemia, aldosteronism, and renal cysts was also supported by the finding of multiple medullary cysts in two patients with primary renal potassium wasting. We conclude that chronic hypokalemia is accompanied by enhanced renal cytogenesis and may lead to interstitial scarring and renal insufficiency. Renal cysts are thus dynamic structures whose growth can be influenced by hormonal or pharmacologic interventions.

Adenoma↗

PubMed1990

Pulmonary fibrosis as an unusual clinical manifestation of a pulmonary-renal vasculitis in elderly patients.

Between 1978 and 1988, three patients at our institution had an initial diagnosis of idiopathic pulmonary fibrosis but later were correctly diagnosed as having pulmonary-renal syndrome and microscopic polyarteritis. These cases involved elderly patients with progressive dyspnea and nonproductive cough, bilateral dry crackling rales, bilateral interstitial infiltrates evident on a chest roentgenogram, and restrictive findings on pulmonary function testing. In two patients, lung biopsy specimens were obtained, and an initial diagnosis of nonspecific pulmonary fibrosis was made. All three patients eventually had microhematuria and renal insufficiency. A revised diagnosis of small-vessel pulmonary-renal vasculitis was based on the demonstration of segmental necrotizing glomerulonephritis in renal biopsy specimens in two patients, thrombotic microangiopathy consistent with healed vasculitis on postmortem examination of the kidney in one patient, and subsequent detection of small-vessel vasculitis on review of the two lung biopsy specimens. Anti-neutrophil cytoplasmic antibodies with perinuclear staining on indirect immunofluorescence microscopy were positive in the two patients in whom determinations were performed. The clinical manifestations of vasculitis were notably scarce--no involvement of the skin, nervous system, or gastrointestinal tract; no episodes of fever; and minimal or absent musculoskeletal symptoms. These cases illustrate the importance of a high index of suspicion for the diagnosis of systemic vasculitis in elderly patients and the need to consider a vasculitis in the differential diagnosis of idiopathic pulmonary fibrosis, especially if an active urinary sediment is present.

Aged↗

PubMed1990

Hepatic cyst infection in autosomal dominant polycystic kidney disease.

To characterize the syndrome of hepatic cyst infection in autosomal dominant polycystic kidney disease (ADPKD) and to review its diagnosis and management, we retrospectively studied five such cases in patients from our institution and nine detailed case reports from the literature. The clinical manifestations were an acute (58%) or subacute (42%) febrile illness, typically associated with tenderness in the right upper quadrant, leukocytosis, a very high erythrocyte sedimentation rate, but minor abnormalities of liver function tests. Bacteremia was present in 7 of 11 patients. Enterobacteriaceae grew in pure culture from the cyst fluid in 9 of 12 patients. Complex cysts were observed by ultrasonography (in four of eight patients), computed tomography (in six of nine), and magnetic resonance imaging (in two of two). 111In leukocyte scans were positive in all four patients in whom they were done, and 67Ga scans were positive in only one of three patients. An unfavorable outcome was observed in six of seven patients treated with only antibiotics, in contrast with one of seven patients who received antibiotics and early drainage. In two patients, ciprofloxacin cyst levels were 2.3 and 4.8 times higher than the level in serum; in a third patient, cyst levels remained in therapeutic range 30 hours after the last dose of ciprofloxacin, at which time serum levels were undetectable. Clinical and laboratory features and the use of modern scanning techniques facilitate a prompt diagnosis of infection in hepatic cysts in ADPKD. The treatment of choice is a combination of percutaneous drainage and antimicrobial therapy.

Aged↗

PubMed1990

Long-term outcome of renal transplantation in autosomal dominant polycystic kidney disease.

This study was performed to determine the long-term outcome of renal transplantation in 54 patients with end-stage renal failure secondary to autosomal dominant polycystic kidney disease (ADPKD) and in 107 patients with renal diseases other than ADPKD or diabetes mellitus matched by gender, age, year of transplantation, and source of the allograft. The overall patient survival and patient survival with a functioning first renal allograft were similar in both groups. Infection and cardiovascular accidents were the leading causes of early and late death in both groups. No cause of death was greatly overrepresented in the ADPKD group. Serious complications from extrarenal manifestations of ADPKD following renal transplantation included a ruptured intracranial aneurysm in one patient, a dissection of the ascending thoracic aorta in one patient, and infected hepatic cysts in two patients. Neoplasia (other than skin or cervical) occurred in four ADPKD patients and in one control patient and included one lymphoma in each group. Two ADPKD and one control patient had monoclonal gammopathies of undetermined significance. No complications related to the retention of native kidneys were detected in 12 ADPKD patients with a mean follow-up of 3 years. Cysts were observed in the renal allografts of some patients in both groups at autopsy and in a prospective computed tomography (CT) study of the allograft. However, we failed to detect a significant difference in the occurrence and number of the cysts between ADPKD and control patients.

Adult↗

PubMed1990

Treatment of highly symptomatic polycystic liver disease. Preliminary experience with a combined hepatic resection-fenestration procedure.

Polycystic liver disease (PLD) associated with autosomal dominant polycystic kidney disease is usually well tolerated. However there is a small subset of patients who become incapacitated by massive liver enlargement and for whom effective nonsurgical therapy is limited. Recent surgical advances in the treatment of PLD have raised uncertainties regarding proper management of these highly symptomatic patients. We have reviewed our recent experience with a combined hepatic resection-fenestration procedure to assess its efficacy in nine patients. All patients underwent resection of two or more liver segments and extensive fenestration of residual cysts in the remnant liver. Symptomatic relief and reduction in abdominal girth were obtained in eight surviving patients, persisting for an average follow-up period of 17 months. No progression of cystic disease has been observed clinically or by computed tomography and hepatic function was preserved. Three patients had no complications. Five patients had complications including transient right pleural effusion (3) and thrombosis of an arteriovenous fistula (2). One patient who had a previous hepatic cyst fenestration and a cadaveric renal transplantation died after operation of an intracerebral hemorrhage after experiencing coagulopathy, hyperbilirubinemia, and sepsis. Our results suggest (1) some highly symptomatic patients with massive PLD may benefit from combined hepatic resection and fenestration with acceptable risk, and (2) previous liver surgery and immunosuppressive therapy may increase the risk of such surgery. Longer follow-up is needed in a larger number of patients to determine the duration of benefit from the combined resection-fenestration procedure for highly symptomatic PLD.

Adult↗

PubMed1990

Cranial computed tomography and magnetic resonance imaging in autosomal dominant polycystic kidney disease.

High resolution computed tomography or magnetic resonance imaging of the head with 3-mm sections through the circle of Willis was obtained in 96 patients with autosomal dominant polycystic kidney disease. These scans are well suited for the noninvasive, presymptomatic diagnosis of intracranial aneurysms at high risk of rupture, since the risk of rupture of unruptured aneurysms is heavily dependent on their size, and aneurysms equal to or larger than 6 mm in diameter are not likely to escape detection by these techniques. No definite aneurysm was observed in any of the 96 patients. Small areas (2-4 mm) of contrast enhancement or signal void were detected in 11 patients. These areas are possibly due to vascular tortuosity, but the studies were considered to be indeterminate because a small aneurysm could not be ruled out. Cerebral angiography in two of these 11 patients was normal. Arachnoid cysts were observed more frequently in the patients with polycystic kidney disease than in a control group of patients matched by gender, age, and type and date of examination.

Adult↗

PubMed1990

The liver in autosomal dominant polycystic kidney disease. Implications for pathogenesis.

A histomorphometric and clinico-pathologic analysis of 26 autopsy cases of autosomal dominant polycystic kidney disease (ADPKD) showed that (1) the density of biliary microhamartomas (BMHs) and the stage of polycystic liver disease were strongly correlated, and (2) both were positively correlated with the stage of renal dysfunction and age at autopsy. Using multiple linear regression analysis, only the stage of renal dysfunction was significantly predictive of the density of BMHs, but both variables were simultaneously predictive for the stage of polycystic liver disease. On serial sections, 41.4% of cysts were connected to BMHs and 81.0% of BMHs to portal tracts. Bile-like material was found in 10.7% of BMHs. Flat or polypoid hyperplasia of the epithelium was observed in 2.7% of cysts. These results support the long-maintained view that hepatic cysts in ADPKD result from cystic dilatation of BMHs. They indicate, however, that the number of BMHs increases during life. These observations are consistent with the hypothesis that hepatic and renal cysts in ADPKD have similar pathogeneses, that BMHs and hepatic cysts result from hyperplasia of the bile duct epithelium, and that as they grow, the hepatic cysts become disconnected from the biliary ducts from which they are derived.

Adult↗

PubMed1989

Natriuretic response to volume expansion in polycystic kidney disease.

Hypertension is an early manifestation of autosomal dominant polycystic kidney disease (ADPKD). Whether polycystic kidneys have an intrinsic abnormality that leads to sodium retention, volume expansion, and hypertension is uncertain. We studied the natriuretic response to a 4-hour infusion of physiologic saline at a rate of 6.5 ml/kg per hour in 10 patients with ADPKD who had normal renal function and 10 gender- and age-matched control subjects. Baseline 24-hour urinary excretions of sodium and potassium were similar in both groups. The baseline filtration fraction was significantly higher in the patients with ADPKD than in the control subjects. During the infusion of saline, no significant changes in blood pressure, clearance of inulin, or clearance of p-aminohippuric acid were detected. The increase in fractional excretion of sodium over baseline was significantly higher in the patients with ADPKD than in the control subjects. The pressure-natriuresis regression line was significantly shifted to the right in patients with ADPKD who had hypertension. The fractional excretion of potassium was significantly lower in patients with ADPKD than in control subjects. No significant differences in plasma renin activity, aldosterone, or atrial natriuretic factor were detected between the two groups. These observations suggest the presence of subtle abnormalities in the management of renal sodium that might contribute to the development and maintenance of hypertension in patients with ADPKD.

Adult↗

PubMed1989

Renal insufficiency in community patients with mild asymptomatic microhematuria.

Primary-care physicians often must decide when patients with asymptomatic microhematuria warrant further testing for renal parenchymal disease. Because previous data had shown a greater frequency of elevated serum creatinine concentration in a population with asymptomatic microhematuria than in control subjects without hematuria, we reviewed the records of 125 patients with isolated asymptomatic microhematuria and elevated serum creatinine (AM/EC) and 83 comparison patients with no hematuria and elevated serum creatinine (NH/EC) from a previous population-based study to determine the relationship between renal parenchymal disease and isolated asymptomatic microhematuria. Serum creatinine was often elevated transiently because of volume depletion or shock, or elevations occurred in relationship to a terminal illness. Thus, only 63 AM/EC patients and 45 NH/EC control subjects had primary renal parenchymal disease or systemic disorders that caused an elevated serum creatinine. The patients selected from the asymptomatic microhematuria population because of elevated serum creatinine most often had low-grade hematuria and were typically 75 years of age or older. No disease was consistently found more frequently in the AM/EC patients than in the NH/EC group. Intervention at the time of the detection of hematuria might have altered the prognosis in 8% and probably would not have altered the prognosis in 78%. Therefore, exhaustive diagnostic testing to detect renal parenchymal diseases cannot be advised in asymptomatic elderly patients with low-grade (grade 1) microhematuria unless more specific indications are present.

Adult↗

PubMed1989

Risk factors in idiopathic renal vasculitis and glomerulonephritis.

In this retrospective study, we analyzed clinical laboratory, and pathologic variables to determine their value in predicting survival and survival free of renal failure for 170 consecutive patients with idiopathic renal vasculitis and glomerulonephritis evaluated during a 15 year period. Of the 170 patients, 108 had focal segmental necrotizing glomerulonephritis alone (FSNGN), 33 had FSNGN and small-artery vasculitis, and 29 had FSNGN and medium-sized artery vasculitis. Considerable overlap of clinical, laboratory, and pathologic findings existed among the three groups. Overall patient survival was 81% at one year, 61% at five years, and 44% at ten years, significantly less than expected survival. Overall survival free of renal failure, by definition, was lower than patient survival. There were no differences among these three groups in patient survival or survival free of renal failure. Multivariate analysis identified leukocytosis and serum creatinine level as independent predictors of patient survival and survival free of renal failure. In addition, univariate analysis identified age and hypertension as significant risk factors but did not add independent predictive value for these two end points. In patients with serum creatinine levels less than 4 mg/dl, the effect of increasing levels of leukocyte count was significantly associated with poorer outcomes for both patient survival (P = 0.006) and survival free of renal failure (P = 0.024). Outcomes for these two end points were worse for patients with lower serum creatinine levels (less than 4.0 mg/dl) and high leukocyte counts (greater than 16,000/mm3) than for those with serum creatinine levels greater than or equal to 4.0 mg/dl.

Adult↗

PubMed1989

Eosinophil granule major basic protein in acute renal allograft rejection.

Conventional staining techniques to determine the presence of tissue eosinophils underestimate their number and do not usually detect eosinophil degranulation. We have studied the involvement of eosinophils in acute renal allograft rejection by immunofluorescence localization of eosinophil granule major basic protein (MBP) in the kidney and by measurement of MBP in the plasma and urine by radioimmunoassay. Tissue eosinophilia and extracellular deposition of MBP indicative of eosinophil degranulation were observed in 94% and 87%, respectively, of patients with acute rejection as compared with 17% and 17%, respectively, of patients with cyclosporine nephrotoxicity. The urine levels of MBP were significantly elevated in acute rejection but not in cyclosporine nephrotoxicity. Plasma MBP concentrations were within the normal range in both acute rejection and cyclosporine nephrotoxicity. The presence of marked tissue eosinophilia and eosinophil degranulation did not always indicate irreversible rejection. Interleukin-2 and IL-2 receptors were also elevated in the urine during acute rejection. These results support a role for the eosinophil as an effector of tissue damage during rejection and suggest the potential usefulness of urine MBP determinations for the immunologic monitoring of transplanted patients.

Acute Disease↗

PubMed1988

Acute interstitial nephritis: immunologic and clinical aspects.

Acute interstitial nephritis is a common renal syndrome that may be associated with a variety of infections and drug therapies or may develop without an identified cause. Three cases are presented to illustrate the three types of acute interstitial nephritis--drug related, infection related, and idiopathic. Cell-mediated immune mechanisms seem to be more important than humorally mediated mechanisms in the pathogenesis of acute interstitial nephritis. Frequently, eosinophils are identified as a component of the interstitial cellular infiltrate, and eosinophiluria and eosinophilia have been claimed to be helpful in the diagnosis of acute interstitial nephritis, especially the drug-induced type. Neither eosinophiluria nor the presence of increased urinary levels of eosinophil major basic protein, however, is specific for the diagnosis of acute interstitial nephritis. Patients with drug-induced interstitial nephritis frequently have symptoms and signs suggestive of a hypersensitivity syndrome and rarely have more dramatic anaphylactic manifestations. Systemic glucocorticoids have been shown to be beneficial in this type of acute interstitial nephritis.

Acute Disease↗

PubMed1988

The association of nephrolithiasis and autosomal dominant polycystic kidney disease.

Despite the frequency and morbidity of nephrolithiasis in autosomal dominant polycystic kidney disease (ADPKD), this association has not been subject to a detailed study. One hundred fifty-one of 751 ADPKD patients seen at the Mayo Clinic between 1976 and 1986 had nephrolithiasis. Seventy-four had passed calculi or had stones surgically removed. Stone analysis was available in 30 patients: uric acid, calcium oxalate, calcium phosphate, and struvite were present in 56.6%, 46.6%, 20%, and 10%, respectively. Calculi were observed in 71 of 79 patients with excretory urograms available for review. Faintly opaque and bull's eye stones, probably containing uric acid, were present in 12.7% and 14.1% of these patients, respectively. Precaliceal tubular ectasia was observed in 15.5%. Ninety-seven patients had preserved renal function (serum creatinine less than 1.5 mg/dL) at the initial evaluation. Six were excluded because they had other known causes of stone disease. The most common metabolic abnormality in the remaining 91 patients was hypocitric aciduria (ten of 15 patients with measurements). The urine pH in the first voided morning specimens (5.66 +/- 0.05) was significantly lower than that of an unselected control population (5.92 +/- 0.03, P less than 0.001). Hyperuricosuria, hyperoxaluria, and hypercalciuria were observed in six of 32 (18.8%), six of 31 (19.4%), and three of 39 (9.7%) patients with preserved renal function. The composition of the stones, the frequency of hypocitric aciduria, and the low urine pH (possibly related to the defect in excretion of ammonia described in ADPKD), suggest that metabolic, along with mechanical, factors are responsible for the frequent occurrence of nephrolithiasis in this disease.

Adult↗

PubMed1988

Bilateral hemorrhagic parapelvic pseudocysts.

The development of bilateral parapelvic hemorrhagic pseudocysts with abdominal pain, systemic symptoms of malaise and fever, elevation of erythrocyte sedimentation rate and serum alkaline phosphatase, and decreased renal function is described in a patient taking anticoagulants. The symptoms and signs resolved with the resolution of the hemorrhagic pseudocysts. The bilaterality and selective localization of these hemorrhages suggest the existence of a specific pathogenesis. The advent of new imaging techniques in the last decade allows for a diagnosis and a better understanding of the pathologic processes that affect the renal sinus.

Cysts↗

PubMed1988

Mechanisms affecting the development of renal cystic disease induced by diphenylthiazole.

To provide information on the possible influence that hypertension or its treatment might have on the development of cysts in autosomal dominant polycystic kidney disease, we studied the effects of the sodium content of the diet, DOCA-salt hypertension, renovascular hypertension, and the administration of enalapril or furosemide on the development of 2-amino-4-5-diphenylthiazole (DPT)-induced renal cystic disease. DOCA-salt hypertension caused vascular and glomerular lesions and proteinuria, but it did not enhance the development of cysts. Cytogenesis was enhanced in experimental conditions where the renin-angiotensin system is known to be activated. On the other hand, interventions known to suppress the renin-angiotensin system lessened the development of cysts. We hypothesize that this effect might be mediated by intrarenal angiotensin II and its capacity to promote cell growth and to control the postglomerular vascular resistances and the compliance of the renal interstitium.

Animals↗