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PubMed2004

Mouse model of X-linked Alport syndrome.

X-linked Alport syndrome (XLAS) is a progressive disorder of basement membranes caused by mutations in the COL4A5 gene, encoding the alpha5 chain of type IV collagen. A mouse model of this disorder was generated by targeting a human nonsense mutation, G5X, to the mouse Col4a5 gene. As predicted for a nonsense mutation, hemizygous mutant male mice are null and heterozygous carrier female mice are mosaic for alpha5(IV) chain expression. Mutant male mice and carrier female mice are viable through reproductive age and fertile. Mutant male mice died spontaneously at 6 to 34 wk of age, and carrier female mice died at 8 to 45 wk of age, manifesting proteinuria, azotemia, and progressive and manifold histologic abnormalities of the kidney glomerulus and tubulointerstitium. Ultrastructural abnormalities of the glomerular basement membrane, including lamellation and splitting, were characteristic of human XLAS. The mouse model described here recapitulates essential clinical and pathologic findings of human XLAS. With alpha5(IV) expression reflecting X-inactivation patterns, it will be especially useful in studying determinants of disease variability in the carrier state.

Alleles↗
PubMed2004

Biologic markers for the early detection of acute kidney injury.

PURPOSE OF REVIEW: This review discusses the current status of several biomarkers as potential diagnostic tools in patients with acute kidney disease. RECENT FINDINGS: Although the term "acute renal failure" has generally been used to describe acute kidney dysfunction that runs the spectrum from mild prerenal azotemia with no renal pathologic changes and no functional failure to severe oliguric renal dysfunction associated with tubular necrosis with failure of function, this spectrum is better described by the term "acute kidney injury." The mortality rate of hospitalized patients with severe acute kidney disease has not decreased significantly over the past 50 years despite advances in supportive care. The absence of sensitive and specific biomarkers for detecting injury early, grading the severity of the injury, and monitoring the response to therapy has impaired progress in the field and has had a very detrimental effect on the design and outcome of clinical trials in acute kidney disease. As a result of reliance on serum creatinine as a marker for injury and diagnosis, the institution of therapy is markedly delayed. SUMMARY: The search for new biomarkers for acute kidney injury is evolving rapidly with advancement in modern technologies. With better biomarkers we will have the ability to detect injury earlier, identify subclinical injury, provide prognostic information on the course of renal impairment, identify the nephron segments most affected, provide a rationale for segmentation of patients for clinical studies, guide timing of therapy, assess response to therapy, and screen patients at risk for renal injury.

Acute Kidney Injury↗
PubMed2004

Fetal bladder sagittal length: a simple monitor to assess normal and enlarged fetal bladder size, and forecast clinical outcome.

PURPOSE: We examined if the parameter of fetal bladder sagittal length (FBSL) could serve as a monitor of normative and enlarged fetal bladder size. MATERIALS AND METHODS: There were 76 consecutive cases examined between 1984 and 2000 that included measurement of fetal bladder size as FBSL and postnatal urological followup. Fetal images used to assess normal bladder size were derived from cases in which the bladder was normal on prenatal imaging and postnatal testing. An enlarged bladder was categorized as being greater than the 95% CI for a given gestational age (GA). The presence and extent of renal pelvic dilatation were also noted and correlated with FBSL. RESULTS: Measuring normal FBSL in 39 fetuses showed an exponential growth pattern (r = 0.76), which could be represented by the approximate linear formula FBSL = GA in weeks -5 (+/- 95% upper/lower CI = 7). An enlarged bladder was diagnosed in 37 fetuses. A dilated bladder in 9 fetuses, defined as FBSL greater than the 95% upper CI of normal (ie between GA + 2 and GA + 12), showed outcomes of posterior urethral valves, vesicoureteral reflux or a normal outcome. Megacystis in 28 fetuses, defined as FBSL greater than 10 mm larger than that of a dilated bladder (ie greater than GA + 12), showed additional outcomes of megacystis megaureter/vesicoureteral reflux or prune-belly syndrome. A normal outcome was significantly more likely in fetuses with a dilated bladder than in those with megacystis (p < or = 0.05). The incidence of azotemia in those with a dilated bladder or megacystis and pyelectasis was significantly lower than that in those with megacystis with hydronephrosis (p < or = 0.03). CONCLUSIONS: Postnatal diagnosis of fetuses that show an enlarged bladder is predicted based on whether the bladder is enlarged as a dilated bladder or megacystis and if the renal pelvis is enlarged as pyelectasis or hydronephrosis.

Female↗
PubMedDate not supplied

Degradation of low molecular weight uremic solutes by oral delivery of encapsulated enzymes.

An alginate microcapsule was developed that contains three enzymes (urease, uricase, and creatininase) capable of effectively degrading urea, uric acid, and creatinine, which are elevated to pathologic levels in patients with kidney failure. The capsules were evaluated in vitro and in vivo in a rodent model and evidenced considerable potential as a possible adjunctive therapy in the treatment of ESRD. In vitro, 5 mL of the capsules incorporating a quantity of enzymes in the mg range effectively degraded all the uric acid, 97% of the urea, and 70% of the creatinine within 24 hours in a 100 mL test solution simulating the concentration of these solutes in uremic plasma. Enzyme degradation of urea followed Michaelis-Menten kinetics, and the Lineweaver-Burk plots for both encapsulated enzymes and unencapsulated control animals were superimposable, indicating that mass transfer through the capsules was not rate limiting in the degradation process. A chemically induced acute renal failure model in the rat was used to evaluate the ability of encapsulated enzymes, along with an oral sorbent (ion exchange resin), to degrade uremic toxins in vivo. Encapsulated enzyme therapy decreased the severity of azotemia by as much as 70%. Preliminary scale up calculations indicated that oral delivery to humans would involve a practical and manageable quantity of enzymes. This is the first study using a combination of enzymes in a single delivery vehicle to degrade multiple uremic toxins.

Acute Kidney Injury↗
PubMed2006

Animal models of HIV-associated nephropathy.

PURPOSE OF REVIEW: HIV-1-associated nephropathy is characterized clinically by proteinuria with azotemia and pathologically by collapsing focal segmental glomerulosclerosis with tubulointerstitial nephritis and microcystic tubular dilatation. This review summarizes the manner in which different transgenic animal models contribute to our knowledge of the pathogenesis of HIV-1-associated nephropathy. RECENT FINDINGS: The most widely studied has been a transgenic mouse model bearing a gag and pol-deleted proviral construct that develops renal disease with many of the clinical and pathologic characteristics seen in HIV-1-associated nephropathy. Studies using this model have helped to highlight the role of HIV-1 viral gene expression in renal cells, podocyte dysregulation, and genetic host factors in the pathogenesis of HIV-1-associated nephropathy. This model has provided the key insights that led to detection of HIV-1 in human kidney epithelial cells. Other transgenic models have helped define critical roles for individual HIV gene products (Nef and Vpr) in the pathogenesis of HIV-1-associated nephropathy. Transgenic mouse models have also provided a method to discover new treatments targeting various steps in the pathogenesis of this disease. SUMMARY: Transgenic animal models of HIV-1-associated nephropathy have contributed greatly to the progress made toward understanding the pathogenesis of this disease.

AIDS-Associated Nephropathy↗
PubMed2005

The role of ultrasound in renal insufficiency: the essentials.

Sonography is the best screening modality to evaluate patients presenting with renal insufficiency. Ultrasound findings can be normal in patients with renal disease, especially in prerenal azotemia and acute parenchymal renal disease. Echogenic kidneys indicate the presence of parenchymal renal disease; the kidneys may be of a normal size or enlarged. Small kidneys suggest advanced stage chronic kidney disease. Uncommonly, cystic disease of the kidney, especially adult type polycystic kidney disease may be the cause of the patient's renal insufficiency with bilaterally enlarged kidneys containing multiple cysts of various sizes. If hydronephrosis is present, the level and cause of the obstruction should be sought. When ultrasound cannot diagnose the level and cause of obstruction, other imaging modalities, including CT and MRI may be useful. When renovascular disease (arterial stenosis or venous thrombosis) is suspected, spectral and color Doppler can be useful in detecting abnormalities.

Education, Medical, Continuing↗
PubMed1986

Effects of ACE inhibition on renal regulation of salt and water.

CHF may activate the RAS by various mechanisms. Acute CHF is associated with high PRA, whereas chronic, stable disease is combined with normal values. The response to ACEI is affected by blood pressure, degree of activation of the RAS, salt balance and degree of possible renal failure. It may also be affected by concomitant diuretic or, e.g., digoxin therapy. ACEI improves RPF, GFR may remain normal or may increase, if it was previously impaired due to reduced RPF. Severe hypotension in combination with decreased autoregulatory capacity may decrease GFR. Generally, renal excretion of sodium and water increase. These changes in renal handling of salt and water are primarily caused by decreased AII. They are also augmented by inhibited sympathetic tone and thirst and decreased release of ADH and aldosterone. Increased synthesis of vasodilating and natriuretic PGs is probably also of some importance. Dilutional hyponatremia may be corrected by combined ACE inhibitor and furosemide treatment. Water and sodium excretion increase and sodium is redistributed from the intracellular space. Low serum sodium values increase and azotemia may be corrected, if ACE inhibitor doses are carefully titrated to avoid severe hypotension. These effects are ascribed mainly to a decrease of AII, thirst and ADH release. The effect of furosemide is improved since increased amounts of salt are delivered to the loop of Henle and access of furosemide to its site of action is facilitated by increased RPF. ACEI does not cause any obvious negative effects on renal handling of salt and water.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1991

Familial juvenile nephronophthisis in two siblings--histological findings at an early stage.

We present two female siblings with familial juvenile nephronophthisis (FJN) which was diagnosed at the early stage of renal failure. Diagnosis was made during the investigation of anemia in case 1 and by a subsequent family survey in case 2. Most patients with FJN are not identified until the terminal stage of renal failure and such cases have rarely been reported in Japan. Case 2 had a reduction in the maximum urinary concentration ability but no azotemia, and among the FJN patients reported in Japan so far she has the least advanced renal disease. Histological examination of the renal biopsy in case 1 showed typical findings of FJN, such as thickening and lamination of the tubular basement membrane (TBM), interstitial fibrosis, and round cell infiltration of the interstitium. In case 2, renal biopsy revealed an irregular marked thickening of the TBM with trivial interstitial changes and a normal glomerular appearance. The histology of these two cases suggests that the TBM may be the primary site affected in FJN.

Child↗
PubMed1983

A simple aid to the differential diagnosis of oliguria.

A study was conducted in oliguric and acutely azotemic patients, measuring: (i) the fractional excretion of sodium (FENa) using creatinine clearance as a measure of glomerular filtration rate, and (ii) sodium clearance relative to urea clearance, designated as the sodium/urea clearance ratio (Na:urea CR). It was found that FENa discriminated between "tubular" and "non-tubular" disorders in 96% of patients. Further, Na:urea CR was as discriminating as FENa. Patients with Na:urea CR above 2.5% can be reliably diagnosed as having acute tubular necrosis or acute urinary tract obstruction; those with a value less than 2.5% will have acute glomerulonephritis or pre-renal azotemia. As urea and sodium measurements are so readily available, this test can now be applied in the assessment of the oliguric or acutely azotemic patient in any hospital practice.

Acute Kidney Injury↗
PubMed1988

A prospective randomised trial of cyclosporin versus methotrexate after HLA-identical sibling marrow transplantation for patients with acute leukemia in first remission: analysis 2.5 years after last patient entry.

The results of a prospective randomised trial comparing cyclosporin (CSP) with methotrexate (MTX) as immunosuppressive therapy after HLA-identical sibling marrow transplantation for patients with acute leukemia in first remission were analysed 2.5 years after entry of the last patient into the trial. Patients given cyclosporin showed a faster rate of marrow engraftment, less oro-pharyngeal mucositis, more azotemia and more diastolic hypertension than those receiving methotrexate. Actuarial four-year survival was 69% for patients receiving MTX and 43% for those receiving cyclosporin (not significant). Actuarial four-year survival in continuous complete remission from the time of transplant was 69% and 38% respectively (not significant, p = 0.09). While there was no difference in the incidence or severity of acute or chronic graft-versus-host disease, the actuarial rate of leukemic recurrence was 0% in the MTX and 36% in the GSP group (p = 0.02). This finding emphasises the importance of long-term follow up for the full assessment of new therapeutic protocols of marrow transplantation in the treatment of hematological malignancy.

Adolescent↗
PubMedDate not supplied

Therapy of ocular and visceral leishmaniasis in a cat.

An 8-year-old, spayed female Domestic Short-haired cat was referred for further evaluation of chronic lymphocytic-plasmacytic stomatitis and bilateral ocular disease. The cat had been treated with systemic glucocorticoids for several months. Initial ophthalmic examination revealed bilateral deep stromal corneal ulcers, exudative panuveitis and secondary glaucoma. Mature mild neutrophilia and monocytosis were detected on complete blood cell count. Abnormalities in the serum profile were hyperglycemia, mild azotemia, hyperglobulinemia and moderate polyclonal gammapathy. Urinalysis revealed glucosuria without ketonuria. Diabetes mellitus was diagnosed and treatment with long-acting insulin was started. An enzyme-linked immunosorbent assay was highly positive for leishmaniasis, and treatment with allopurinol was started. Although specific topical treatment was applied, melting ulcers progressed to corneal perforation and both eyes were enucleated. Ocular histology showed large numbers of intracellular organisms compatible with amastigotes of the genus Leishmania located in the uveal tract, cornea, sclera and retina. Results of inmunohistochemistry staining on ocular samples were positive for Leishmania. Bone marrow cytology demonstrated numerous macrophages with intracytoplasmatic Leishmania. Polymerase chain reaction results on bone marrow for Leishmania were positive. Three weeks later, hypoglycemic episodes permitted withdrawal of the insulin therapy. To the authors' knowledge this is the first case of ocular and visceral leishmaniasis diagnosed in vivo and under systemic treatment in a cat.

Allopurinol↗
PubMed2005

Initial Brazilian experience with short-duration in-center daily hemodialysis.

The whole initial Brazilian experience with short-duration in-center daily hemodialysis is summarized here. The study was performed at a time when low-flux membrane and nonproportional dialysis represented the standard dialysis treatment in Brazil. Five patients were treated for 2 years. The subject is developed in a way to narrate the efforts to set the research project and summarize the findings, meeting presentations, and publications that derived from the project. At the end of the study, the main benefits observed consisted of alleviation of the end-stage renal disease anemia; reduction of the frequency of complications during dialysis sessions; a lower degree of azotemia; easier blood pressure control; and improvements in acid-base status, mineral metabolism and bone disease, nutrition, and quality of life.

Acid-Base Equilibrium↗
PubMed1998

Mesangiolytic glomerulopathy in severe congestive heart failure.

To study the glomerular morphological abnormalities in congestive heart failure (CHF), we analyzed 27 autopsy cases without other causes of renal disease. Their mean age was 59 years, and they showed mild prerenal azotemia. They had generally been treated with digitalis and diuretics, and a few of them with captopril or nifedipine. The abnormal glomerular findings of enlargement, hyperemia, and mesangial thickening were observed at high frequencies (61%, 64%, and 57%, respectively). They characteristically showed mesangiolysis (ML) by the findings of microaneurysms (81%) and mesangial degeneration (70%) such as loose reticular matrix and poor matrix area. In addition, glomerular infiltration of mononuclear leukocytes including macrophages was noted in 70% of the cases. Glomerular enlargement was not correlated with the grade of hyperemia, but it was correlated with the grade of ML index of % glomeruli with microaneurysms (F = 7.22, p < 0.004). There was an inverse relationship between the grades of mesangial thickening and of the ML index (P < 0.005). The number of glomerular leukocytes was positively correlated with mean glomerular size (P < 0.002) and with the ML index (P < 0.03). Notably, the glomerular macrophage-positive cases showed a prominently higher mean ML index than the negative cases (P < 0.005). There was an inverse correlation between the mean glomerular size and the partial oxygen pressure in arterial blood (PaO2; P < 0.01), and a positive correlation between the mean glomerular size and hematocrit (Hct) levels (P < 0.02). The cases positive for mesangiolytic mesangial degeneration showed significantly lower PaO2 values than the cases negative for this lesion (P < 0.04). In the analysis of the various causes of CHF, the patients with congenital cardiac anomalies showed mean levels of the lowest PaO2 (P < 0.02) and the highest Hct (P < 0.03) and histologically the largest mean glomerular size (P < 0.04). There was no difference in the ML index and the glomerular leukocyte number among the subgroups classified by the causes. These results indicate that ML associated with glomerular enlargement is the major glomerular abnormality characteristic in patients with severe CHF and suggest that glomerular infiltration of leukocytes, especially of macrophages, should play an important role in the progression of both ML and glomerulomegaly. The contributions of persistent hypoxia and up-regulated angiotensin II as the causative factors of these glomerular abnormalities in congestive heart failure are discussed.

Adult↗
PubMed2005

Dendrimer-enhanced MRI as a diagnostic and prognostic biomarker of sepsis-induced acute renal failure in aged mice.

BACKGROUND: Acute renal failure (ARF) induced by sepsis has a high mortality. In an aged mouse model of sepsis-induced ARF we have previously shown that renal injury occurs before serum creatinine is elevated. Development of a noninvasive biomarker that could diagnose renal dysfunction early in sepsis and monitor the response to therapy would be very valuable. METHODS: We performed magnetic resonance imaging (MRI) with gadolinium-based G4 dendrimer intravenous contrast in a fluid- and antibiotic-treated cecal ligation and puncture (CLP) sepsis model in aged mice. Imaging was also performed in a mouse volume depletion model and in models of ARF induced by ischemia/reperfusion (I/R) and cisplatin. RESULTS: Twenty hours post-CLP, aged mice had a distinct pattern of renal injury using dendrimer-enhanced MRI. This pattern was different from renal injury induced by either cisplatin or I/R. Prerenal azotemia induced by volume depletion was distinguished from sepsis by dendrimer-enhanced MRI. Dendrimer-enhanced MRI detected renal dysfunction 6 hours post-CLP, a time when serum creatinine was still normal. Ethyl pyruvate reversed the renal dysfunction detected by dendrimer-enhanced MRI at 20 hours, but not at 6 hours post-CLP. The appearance of renal dysfunction on dendrimer-enhanced MRI at 6 hours post-CLP predicted the length of survival. CONCLUSION: Dendrimer-enhanced MRI is a novel biomarker that provides information for the early diagnosis, drug responsiveness, and prognosis of sepsis-induced ARF.

Acute Kidney Injury↗
PubMed2005

Early treatment with cGMP phosphodiesterase inhibitor ameliorates progression of renal damage.

BACKGROUND: Chronic renal disease is associated with oxidative stress and reduced nitric oxide availability which, in turn, promotes hypertension and further progression of renal damage. Most actions of nitric oxide are mediated by cyclic 3',5' guanosine monophosphate (cGMP) which is rapidly degraded by phosphodiesterases (PDE). Therefore, we investigated if inhibition of PDE-5 would retard the progression of chronic renal failure. METHODS: We studied rats with 5/6 nephrectomy treated with sildenafil (2.5 mg/kg(-1)/day(-1)) in two experimental protocols. In the first protocol, we started sildenafil therapy immediately after renal ablation and continued treatment for 8 weeks. Control groups consisted of rats with renal ablation treated with drug-free vehicle and sham-operated rats with and without sildenafil treatment. RESULTS: In these studies, sildenafil treatment prevented hypertension and deterioration of renal function, reduced histologic damage, inflammation and apoptosis, delayed the onset of proteinuria, and preserved renal capillary integrity. In the second protocol we compared sildenafil with losartan (7.5 mg/kg(-1)/day(-1)) and the combination of both drugs in established renal disease, starting these drugs 4 weeks after 5/6 nephrectomy. Delayed sildenafil treatment failed to improve proteinuria and glomerulosclerosis but ameliorated hypertension and azotemia. CONCLUSION: These observations suggest that currently available PDE-5 inhibitors have potential clinical value in the treatment of chronic renal disease.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1977

The renal lesion associated with total lipodystrophy.

This report concerns a 41-year-old man with total lipodystrophy associated with a specific renal disorder. He had massive proteinuria, mild azotemia and a normal level of serum complement in addition to the generalized loss of subcutaneous fatty tissue. Results of 1 50-gm glucose tolerance test indicated a high fasting insulin level with an exaggerated response to glucose. Hypoglycemic responses to exogenous insulin were reduced. Renal biopsy revealed changes consistent with glomerular lipidosis. This case is unique in that the renal lesion was not the Kimmelstiel-Wilson pathologic change atributable to abnormal glucose metabolism.

Adult↗
PubMed1982

Reversible intellectual impairment: an internist's perspective.

A review of the relevant literature was stimulated by recent publications urging extensive laboratory assessment of elderly patients presenting with intellectual impairment. Published data regarding reversible causes of impairment are limited and exist only for hospitalized patients, with rare exceptions. The frequencies of azotemia, hyponatremia, volume depletion, hypoglycemia, cardiac arrhythmia, cerebrovascular disease, sensory impairment, hypercarbia, congestive heart failure, infections, subdural hematoma, and chemical intoxications as causes of the intellectual impairment are entirely unknown. It is reported that 8 per cent of patients hospitalized for dementia are depressed; alcoholism is causative in 8 to 13 per cent of patients with mental impairment; normal pressure hydrocephalus is reported in 7 to 12 per cent. The frequency of the latter conditions in outpatients is not known. While estimates exist for the frequencies of hypothyroidism, hyperparathyroidism, neurosyphilis, and vitamin B12 and folate deficiencies among the elderly, no prevalence data exist for these disorders among the intellectually impaired.

Aged↗
PubMedDate not supplied

Postoperative myositis in a neonatal foal: a case report.

A foal with azotemia, acidemia, and electrolyte abnormalities was diagnosed with uroperitoneum. The foal was anesthetized with isoflurane, and throughout the 4 hours of anesthesia and abdominal surgery, its mean arterial pressure ranged between 45 and 65 mm Hg. The foal developed a myopathy postoperatively and died 24 hours after surgery.

Animals↗