Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 20 de 24
Filter
1.
Clin Lab Haematol ; 27(6): 391-4, 2005 Dec.
Article in English | MEDLINE | ID: mdl-16307541

ABSTRACT

We report a 47-year-old man with myelofibrosis who presented with bilateral nephromegaly secondary to extramedullary haematopoiesis. We discuss diagnosis and treatment of this rare case and review the literature.


Subject(s)
Hematopoiesis, Extramedullary , Kidney Diseases/diagnosis , Primary Myelofibrosis/diagnosis , Cell Transformation, Neoplastic , Humans , Hypertrophy/etiology , Kidney Diseases/therapy , Leukemia, Myeloid, Acute , Male , Middle Aged , Primary Myelofibrosis/therapy
2.
QJM ; 97(5): 297-301, 2004 May.
Article in English | MEDLINE | ID: mdl-15100424

ABSTRACT

BACKGROUND: Microscopic haematuria without proteinuria is a common clinical finding. When urological causes are excluded, usual findings on renal biopsy are IgA nephropathy (which can progress to end-stage renal failure) or thin basement membrane nephropathy (which has an excellent prognosis). A non-invasive test to discriminate between the two would be useful. AIM: To examine the value of measurement of urinary albumin excretion in discriminating glomerular causes of microscopic haematuria in patients without proteinuria on urine dipstick tests. DESIGN: Single-centre retrospective cross-sectional observational study. METHODS: Adult patients who underwent renal biopsy for microscopic haematuria over a 6-year period from January 1994 were identified. Study entry required normal renal function, no proteinuria detected by dipstick, and urinary albumin excretion <300 mg/24 h. Patients with IgA nephropathy had follow-up for a mean of 58 months after biopsy. RESULTS: Of 169 patients fulfilling study criteria, 119 (70%) had normoalbuminuria (<30 mg/24 h); 52 (30%) had microalbuminuria (30-299 mg/24 h). Of those with normoalbuminuria, 106 (89%) had thin basement membrane nephropathy or no glomerular abnormality. Thirteen (11%) had IgA nephropathy, and of 12 of these followed-up for a mean 64 months, none developed overt, dipstick-positive proteinuria. In contrast, 24 (48%) of those with microalbuminuria had IgA nephropathy, and of 22 followed-up for a mean 55 months, five developed overt proteinuria. DISCUSSION: Urinary albumin excretion is an indicator of likely glomerular findings in microscopic haematuria, and may influence whether a renal biopsy is necessary.


Subject(s)
Albuminuria/etiology , Glomerulonephritis, IGA/complications , Glomerulonephritis, Membranous/complications , Hematuria/etiology , Adult , Cross-Sectional Studies , Diagnosis, Differential , Disease Progression , Female , Glomerulonephritis, IGA/diagnosis , Glomerulonephritis, Membranous/diagnosis , Humans , Male , Middle Aged , Prognosis , Proteinuria/etiology , Retrospective Studies
3.
J Hosp Infect ; 54(4): 272-8, 2003 Aug.
Article in English | MEDLINE | ID: mdl-12919757

ABSTRACT

Sixty coagulase-negative staphylococcus (CNS) isolates were recovered from the blood cultures or peritoneal dialysate effluent of 43 patients on renal dialysis. The patients had either renal dialysis catheter-related sepsis (CRS) or continuous ambulatory peritoneal dialysis (CAPD)-associated peritonitis. Isolates were characterized by biotyping, and genotyped by pulsed-field gel electrophoresis (PFGE). Phenotypic properties of the strains were also investigated. Several genotypes were identified with no one specific strain of CNS being associated with CRS. However, closely related strains were isolated from several patients within the units studied, suggesting horizontal transfer of micro-organisms. Genotypic macro-restriction profiles did not concur with phenotypic profiles or biotypes, confirming that genotyping is required for epidemiological studies. All staphylococcal strains were investigated for the production of phenotypic characteristics. Significant differences were predominantly seen in the production of lipase, esterase and elastase in strains isolated from the renal patients with CRS and CAPD-associated peritonitis, compared with a non-septic control group. These phenotypic characteristics may therefore have a role in the maintenance of CRS in renal patients.


Subject(s)
Catheters, Indwelling/adverse effects , Cross Infection/microbiology , Peritoneal Dialysis/adverse effects , Staphylococcal Infections/microbiology , Staphylococcus epidermidis/genetics , Staphylococcus hominis/genetics , Adult , Aged , Aged, 80 and over , Bacterial Typing Techniques , Case-Control Studies , Coagulase , Cross Infection/epidemiology , Cross Infection/etiology , DNA, Bacterial/analysis , DNA, Bacterial/genetics , Electrophoresis, Gel, Pulsed-Field , Esterases/metabolism , Female , Genotype , Humans , Infection Control , Lipase/metabolism , Male , Middle Aged , Pancreatic Elastase/metabolism , Peritoneal Dialysis/instrumentation , Peritonitis/microbiology , Phenotype , Sepsis/microbiology , Staphylococcal Infections/epidemiology , Staphylococcal Infections/etiology , Staphylococcus epidermidis/enzymology , Staphylococcus hominis/enzymology
4.
Science ; 293(5532): 1107-12, 2001 Aug 10.
Article in English | MEDLINE | ID: mdl-11498583

ABSTRACT

Hypertension is a major public health problem of largely unknown cause. Here, we identify two genes causing pseudohypoaldosteronism type II, a Mendelian trait featuring hypertension, increased renal salt reabsorption, and impaired K+ and H+ excretion. Both genes encode members of the WNK family of serine-threonine kinases. Disease-causing mutations in WNK1 are large intronic deletions that increase WNK1 expression. The mutations in WNK4 are missense, which cluster in a short, highly conserved segment of the encoded protein. Both proteins localize to the distal nephron, a kidney segment involved in salt, K+, and pH homeostasis. WNK1 is cytoplasmic, whereas WNK4 localizes to tight junctions. The WNK kinases and their associated signaling pathway(s) may offer new targets for the development of antihypertensive drugs.


Subject(s)
Hypertension/genetics , Mutation , Protein Serine-Threonine Kinases/genetics , Pseudohypoaldosteronism/genetics , Amino Acid Sequence , Base Sequence , Chromosome Mapping , Chromosomes, Human, Pair 12/genetics , Chromosomes, Human, Pair 17/genetics , Cytoplasm/enzymology , Female , Gene Expression Regulation, Enzymologic , Genetic Linkage , Humans , Hypertension/enzymology , Hypertension/physiopathology , Intercellular Junctions/enzymology , Intracellular Signaling Peptides and Proteins , Introns , Kidney Tubules, Collecting/enzymology , Kidney Tubules, Collecting/ultrastructure , Kidney Tubules, Distal/enzymology , Kidney Tubules, Distal/ultrastructure , Male , Membrane Proteins/metabolism , Microscopy, Fluorescence , Minor Histocompatibility Antigens , Molecular Sequence Data , Mutation, Missense , Pedigree , Phosphoproteins/metabolism , Protein Serine-Threonine Kinases/chemistry , Protein Serine-Threonine Kinases/metabolism , Pseudohypoaldosteronism/enzymology , Pseudohypoaldosteronism/physiopathology , Sequence Deletion , Signal Transduction , WNK Lysine-Deficient Protein Kinase 1 , Zonula Occludens-1 Protein
5.
Am J Hum Genet ; 68(1): 219-24, 2001 Jan.
Article in English | MEDLINE | ID: mdl-11085914

ABSTRACT

Familial glomerulocystic kidney disease (GCKD) is a dominantly inherited condition characterized by glomerular cysts and variable renal size and function; the molecular genetic etiology is unknown. Mutations in the gene encoding hepatocyte nuclear factor (HNF)-1beta have been associated with early-onset diabetes and nondiabetic renal disease-particularly renal cystic disease. We investigated a possible role for the HNF-1beta gene in four unrelated GCKD families and identified mutations in two families: a nonsense mutation in exon 1 (E101X) and a frameshift mutation in exon 2 (P159fsdelT). The family members with HNF-1beta gene mutations had hypoplastic GCKD and early-onset diabetes or impaired glucose tolerance. We conclude that there is genetic heterogeneity in familial GCKD and that the hypoplastic subtype is a part of the clinical spectrum of the renal cysts and diabetes syndrome that is associated with HNF-1beta mutations.


Subject(s)
DNA-Binding Proteins/genetics , Kidney Diseases, Cystic/genetics , Mutation/genetics , Transcription Factors/genetics , Adolescent , Adult , Age of Onset , Blood Pressure , Child , Codon, Nonsense/genetics , Creatine/metabolism , DNA Mutational Analysis , Diabetes Complications , Diabetes Mellitus/epidemiology , Diabetes Mellitus/genetics , Exons/genetics , Female , Frameshift Mutation/genetics , Genetic Heterogeneity , Glucose Intolerance/complications , Glucose Intolerance/epidemiology , Glucose Intolerance/genetics , Hepatocyte Nuclear Factor 1-beta , Humans , Infant , Infant, Newborn , Kidney Diseases, Cystic/complications , Kidney Diseases, Cystic/epidemiology , Kidney Diseases, Cystic/metabolism , Male , Middle Aged , Pedigree , Syndrome
6.
Nephrol Dial Transplant ; 15(11): 1782-7, 2000 Nov.
Article in English | MEDLINE | ID: mdl-11071965

ABSTRACT

BACKGROUND: Accounts of renal pathological findings in infective endocarditis are mostly based on studies from many years ago. We reviewed a group of patients with infective endocarditis in the light of modern concepts of renal pathology, including the largest reported series of renal biopsies in this condition. METHODS: Renal tissue was available for retrospective study from 62 patients with confirmed infective endocarditis out of 354 diagnosed with the disease between 1981 and 1998 inclusive. Twenty patients had a renal biopsy and 42 a necropsy. RESULTS: Common renal lesions noted were localized infarcts in 31%, noted only in necropsy material, and acute glomerulonephritis in 26%, noted in biopsy and necropsy material. The commonest type of glomerulonephritis was vasculitic, without deposition of immunoproteins in glomeruli. Of the renal infarcts over half were due to septic emboli, mostly in patients infected with Staphylococcus aureus. Acute interstitial nephritis was found in 10% but was more common in biopsy material and seemed attributable to antibiotics. Renal cortical necrosis found in 10% was apparent only at necropsy. There were various other findings in the kidney. CONCLUSIONS: The kidneys are commonly affected in infective endocarditis by a variety of complications of clinical significance. The commonest type of glomerulonephritis does not appear to be attributable to deposition of immune complexes. A renal biopsy may be helpful in the investigation of renal impairment in a patient with infective endocarditis.


Subject(s)
Endocarditis, Bacterial/pathology , Kidney/pathology , Adult , Aged , Biopsy , Female , Glomerulonephritis/etiology , Glomerulonephritis/pathology , Humans , Infarction/pathology , Kidney/blood supply , Male , Medical Records , Middle Aged , Retrospective Studies , Staphylococcal Infections/pathology , Tricuspid Valve
7.
J Pathol ; 190(4): 478-83, 2000 Mar.
Article in English | MEDLINE | ID: mdl-10699998

ABSTRACT

A distinctive segmental glomerular abnormality is confined to the region of the tubular opening. The hypothesis was that this followed prolapse of the tuft into the tubule. Analysis was made of 39 renal biopsy specimens with acute postinfective glomerulonephritis, later material from ten cases, four specimens from three women with pre-eclampsia, and 21 control specimens, with morphometry of glomeruli and immunohistological examination for immunoproteins and monocytes/macrophages. Prolapse was found in 14 specimens with acute postinfective glomerulonephritis, associated in eight with adhesion to Bowman's capsule and local alterations in the tuft, which together constitute early tip changes. Another three had early tip changes only and eight others had thin adhesions between the tuft and capsule next to the tubular opening. Later material confirmed this order of development and showed another late change, with sclerosed and hyaline material in the tuft and adhesion at the tubular origin. Findings in pre-eclampsia were comparable. Glomeruli were significantly larger in acute postinfective glomerulonephritis than in controls and were shown by others to be larger in pre-eclampsia than in normal pregnancy. Immunohistology showed IgM and a few foamy monocytes/macrophages in early tip changes but not in prolapsed loops. Glomerular prolapse appears to be a temporary consequence of acute enlargement of the tuft, probably causes mechanical damage to epithelial cells, and is a precursor of permanent structural changes near the tubular origin. This gives a unifying hypothesis to explain how these changes can be seen in acute postinfective glomerulonephritis, pre-eclampsia, and many other human and experimental renal disorders.


Subject(s)
Glomerulosclerosis, Focal Segmental/pathology , Kidney Glomerulus/pathology , Acute Disease , Adolescent , Adult , Aged , Female , Glomerulonephritis/pathology , Glomerulosclerosis, Focal Segmental/microbiology , Humans , Male , Middle Aged , Pre-Eclampsia/pathology , Pregnancy , Prolapse
8.
J Hum Hypertens ; 13(4): 217-20, 1999 Apr.
Article in English | MEDLINE | ID: mdl-10333337

ABSTRACT

Atherosclerotic renal artery stenosis (ARAS) is the commonest cause of secondary hypertension and is the cause of end stage renal failure in up to 20% of patients starting dialysis. Associated with it is a high morbidity and appalling mortality. The aetiology of ischaemic nephropathy is complex and is not simply related to renal artery narrowing. Captopril renography is sensitive and specific for diagnosing ARAS in patients with normal renal function. In those with renal impairment gadolinium-enhanced MRA or spiral CT angiography clearly define renal anatomy. Over 80% of ARAS is ostial. Studies of revascularisation with angioplasty show poor short and long term patency rates. Renal artery stenting leads to high initial technical success and long term patency. Recent randomised controlled trials in patients with renovascular hypertension demonstrate no clear benefit of adequate revascularisation over medical therapy. Renal artery stenting for renal protection in ARAS appears more encouraging and current randomised controlled trials are in progress to answer the question definitively.


Subject(s)
Arteriosclerosis/diagnosis , Renal Artery Obstruction/diagnosis , Angioplasty , Arteriosclerosis/complications , Arteriosclerosis/therapy , Diagnosis, Differential , Disease Progression , Humans , Hypertension, Renal/diagnosis , Hypertension, Renal/etiology , Hypertension, Renal/therapy , Kidney Failure, Chronic/diagnosis , Kidney Failure, Chronic/etiology , Kidney Failure, Chronic/therapy , Magnetic Resonance Angiography , Radioisotope Renography , Renal Artery Obstruction/complications , Renal Artery Obstruction/therapy , Renal Dialysis , Tomography, X-Ray Computed
10.
Transplantation ; 66(1): 59-66, 1998 Jul 15.
Article in English | MEDLINE | ID: mdl-9679823

ABSTRACT

BACKGROUND: Liver transplant recipients are at risk of chronic renal disease, principally as a result of nephrotoxicity of the commonly used immunosuppressive agents cyclosporine and tacrolimus. We have investigated the incidence of chronic renal failure and its risk factors in our transplant population, which was treated predominantly with cyclosporine. METHODS: A single-center retrospective study was done of 883 consecutive adult patients receiving a first liver transplant between 1982 and 1996. Potential risk factors for the development of chronic renal failure were recorded, including serial measurements of cyclosporine therapy and renal function. RESULTS: Severe chronic renal failure (serum creatinine level >250 microM/L for at least 6 months) developed in 25 patients, representing 4% of patients surviving 1 year or more. Twelve of these patients developed end-stage renal failure and mortality was 44%. The predominant cause of renal failure was cyclosporine nephrotoxicity. Serum creatinine as early as 3 months after surgery was strongly associated with the eventual development of severe chronic renal failure (P=0.001), and this group could be further subdivided into two groups with differing risk factors. The first group had early (<1 year) renal dysfunction, with older age (P=0.03), cytomegalovirus infection (P=0.03), need for perioperative renal replacement therapy (P=0.06), and regrafting (P=0.06) as risk factors for eventual renal failure; the second group had late-onset (>1 year) renal dysfunction, with cyclosporine levels at 1 month after surgery (P=0.007) and daily and cumulative cyclosporine dosage at 5 years (P=0.01 for both) as risk factors. CONCLUSIONS: With improved survival of liver transplant recipients, chronic renal failure has become an important cause of morbidity and is associated with a high mortality. Many patients at risk of severe chronic renal failure may be identified at an early stage. Treatment regimens that avoid or prevent cyclosporine-induced nephrotoxicity are urgently required for this population.


Subject(s)
Kidney Failure, Chronic/etiology , Liver Transplantation , Postoperative Complications , Adolescent , Adult , Aged , Cyclosporine/administration & dosage , Cyclosporine/adverse effects , Cyclosporine/therapeutic use , Dose-Response Relationship, Drug , Female , Humans , Immunosuppressive Agents/administration & dosage , Immunosuppressive Agents/adverse effects , Immunosuppressive Agents/therapeutic use , Incidence , Kidney/drug effects , Kidney/physiopathology , Kidney Failure, Chronic/chemically induced , Kidney Failure, Chronic/epidemiology , Male , Middle Aged , Retrospective Studies , Risk Factors , Tacrolimus/therapeutic use , Time Factors
12.
Transplantation ; 64(7): 1007-17, 1997 Oct 15.
Article in English | MEDLINE | ID: mdl-9381523

ABSTRACT

BACKGROUND: Atrial natriuretic peptide and cyclosporine have opposing effects on renal hemodynamics and excretory function. METHODS: Twelve male stable cyclosporine-treated renal transplant recipients received a single 100-mg i.v. dose of the neutral endopeptidase EC 24.11 inhibitor candoxatrilat in a double-blind, placebo-controlled cross-over study. Each study day consisted of 2 hr of baseline and 7 hr of postdose evaluation. RESULTS: After administration of candoxatrilat, plasma atrial natriuretic factor rose from 12.8+/-1.6 (mean +/- SEM) to 44.1+/-6.8 pmol/L (P<0.001) in association with a threefold increase in urine cGMP excretion (573+/-195 pmol/min baseline to 1823+/-545 pmol/ min; P<0.001), marked natriuresis (207+/-34 micromol/min baseline to 416+/-62 micromol/min; P<0.001), fractional sodium excretion (3.3+/-0.5% baseline to 5.6+/-0.7%; P<0.01), and diuresis (3.4+/-0.5 ml/min baseline to 7.4+/-1 ml/min; P<0.001). All parameters remained elevated above baseline for the remaining 7-hr study period. In response to candoxatrilat, the glomerular filtration rate rose by 19% (P=0.01), renal plasma flow by 7% (P=0.04), renal blood flow by 13% (P=0.03) in association with an increase in filtration fraction from 24+/-2% to 28+/-2% (P=0.002) and small fall in renal vascular resistance from 0.38+/-0.04 to 0.30+/-0.04 mmHg x min x 1.73 m2 x ml(-1) (P=0.02). There was a fall in plasma angiotensin II without a change in plasma renin concentration or plasma aldosterone. Median urinary albumin excretion increased after candoxatrilat administration from 48 (3-131) to 114 (32-641) microg/min (P<0.01). CONCLUSIONS: Acute neutral endopeptidase inhibition with candoxatrilat appears to reverse the adverse renal hemodynamic and renal excretory effects of cyclosporine in stable renal transplant recipients.


Subject(s)
Cyclohexanecarboxylic Acids/therapeutic use , Cyclosporine/adverse effects , Immunosuppressive Agents/adverse effects , Kidney Transplantation/pathology , Kidney Transplantation/physiology , Neprilysin/antagonists & inhibitors , Protease Inhibitors/therapeutic use , Adult , Aged , Atrial Natriuretic Factor/blood , Blood Pressure/drug effects , Cross-Over Studies , Cyclic GMP/blood , Diuresis/drug effects , Double-Blind Method , Drug Therapy, Combination , Glomerular Filtration Rate/drug effects , Humans , Immunosuppressive Agents/therapeutic use , Kidney Transplantation/immunology , Male , Middle Aged , Regional Blood Flow/drug effects , Renal Circulation/drug effects , Sodium/urine , Vascular Resistance/drug effects
13.
Kidney Int ; 52(3): 792-801, 1997 Sep.
Article in English | MEDLINE | ID: mdl-9291201

ABSTRACT

Atrial natriuretic factor (ANF) has natriuretic, renin-suppressing and chronic hypotensive actions that may be utilized by inhibition of ANF degradation by neutral endopeptidase, E.C.24.11 (NEP). Three groups of 8 male patients [GFR 103 +/- 8 (Normal), 64 +/- 6 (Moderate CRF), and 16 +/- 2 ml/min (Severe CRF)] received 100 mg i.v. bolus of the NEP inhibitor candoxatrilat or placebo in random order in a double-blind crossover study. GFR (51CR-EDTA), ERPF (125I-hippuran). ANF (IRMA), urinary cGMP (RIA) and albumin (RIA) and sodium excretion and flow rate were measured hourly for two hours before and for seven hours after candoxatrilat administration. After candoxatrilat plasma ANF rose two- to threefold from baseline, and remained elevated for 5(N) and 7(M,S) hours (P < 0.01(N,S), P < 0.03(M)) associated with an immediate rise in urine cGMP excretion from 23.5(N), 25.4(M) and 10.4(S) nmol/hr (base) to 51.7(N), 73.8(M) and 27.5(S)(peak) lasting 7(N,M,S) hours (P < 0.01(N,M,S)). There was a marked natriuresis in all three groups, the cumulative sodium excretion at seven hours post-candoxatrilat being 104(N), 140(M), 102(S) mmol (P < 0.05(N,M,S)). This was greatest in those with moderate CRF (moderate CRF vs. normal, P = 0.036, moderate vs. severe CRF, P = 0.01, normal vs. severe CRF, P = 0.74). Following candoxatrilat there was a near doubling of the urine flow rate (P < 0.01(N,S), P < 0.02(M)). Urine albumin excretion increased in patients with renal failure (P < 0.01), but there was no change in GFR, ERPF or systemic blood pressure. We conclude that the marked natriuretic effects of acute NEP inhibition seen in normal subjects are enhanced in the presence of moderate CRF and sustained even in severe renal impairment.


Subject(s)
Cyclohexanecarboxylic Acids/therapeutic use , Kidney Failure, Chronic/drug therapy , Kidney Failure, Chronic/physiopathology , Natriuresis/drug effects , Neprilysin/antagonists & inhibitors , Protease Inhibitors/therapeutic use , Adult , Aged , Albuminuria/urine , Atrial Natriuretic Factor/blood , Cross-Over Studies , Cyclic GMP/urine , Diuresis/drug effects , Double-Blind Method , Hemodynamics/drug effects , Humans , Kidney Failure, Chronic/urine , Male , Middle Aged , Renal Circulation/drug effects
14.
J Hypertens ; 11(4): 439-42, 1993 Apr.
Article in English | MEDLINE | ID: mdl-8390512

ABSTRACT

OBJECTIVES: First, to determine the relationship between left ventricular mass (LVM) and clinic and 24-h ambulatory blood pressure parameters in normotensive renal transplant recipients. Secondly, to assess the influence of immunosuppression protocol on diurnal blood pressure and target-organ response. DESIGN: Measurement of supine clinic blood pressure, non-invasive 24-h ambulatory blood pressure and echocardiographically determined LVM. PATIENTS: Twenty-eight stable, normotensive renal transplant recipients taking no antihypertensive therapy (16 cyclosporin-treated and 12 non-cyclosporin-treated). SETTING: Community-based ambulatory patients reviewed in tertiary referral centre. MAIN OUTCOME MEASURES: Clinic blood pressure, mean 24-h, daytime and night-time ambulatory blood pressure and LVM. RESULTS: Mean 24-h blood pressure exceeded that recorded in the clinic. Twenty-five per cent of patients had left ventricular hypertrophy despite the absence of hypertension, and this was more common in cyclosporin-treated than in non-cyclosporin-treated patients. Mean daytime systolic blood pressure was the best predictor of LVM, being superior to clinic blood pressure and any diastolic blood pressure parameter. An attenuated nocturnal blood pressure fall ('non-dipper' pattern) was common, especially in those patients treated with cyclosporin, and was associated with higher LVM. CONCLUSION: In normotensive renal transplant recipients, a group at risk of cardiovascular disease, 24-h ambulatory blood pressure is closely related to the development of left ventricular hypertrophy, and may prove useful in optimizing treatment strategies to reduce cardiovascular morbidity.


Subject(s)
Blood Pressure , Cyclosporine/therapeutic use , Kidney Transplantation/physiology , Myocardium/pathology , Blood Pressure Monitors , Cardiovascular Diseases/etiology , Female , Heart Ventricles/pathology , Humans , Kidney Failure, Chronic/complications , Kidney Failure, Chronic/physiopathology , Kidney Failure, Chronic/surgery , Kidney Transplantation/adverse effects , Kidney Transplantation/pathology , Male , Middle Aged
17.
Nephrol Dial Transplant ; 8(4): 357-60, 1993.
Article in English | MEDLINE | ID: mdl-8390012

ABSTRACT

Musculoskeletal syndromes are common in patients treated by dialysis for end-stage renal failure and abnormal connective tissue metabolism has been implicated. Hyaluronic acid is a major component of connective tissue ground substance. Serum, dialysate, and 24-h urine hyaluronic acid was therefore measured in 43 patients treated by CAPD to determine hyaluronic acid metabolism and to relate these variables to morbidity and mortality over an 18-month period. Serum hyaluronic acid was elevated in 71% patients, being correlated with patient age, length of time on dialysis, and weight loss over the preceding 6 months. Small quantities of predominantly low-molecular-weight hyaluronic acid were lost in the urine, whereas much larger amounts of mixed-molecular-weight hyaluronic acid were excreted in peritoneal dialysate. Dialysate hyaluronic acid exceeded serum hyaluronic acid. Baseline serum hyaluronic acid was closely correlated with morbidity and mortality over the following 18 months. Serum hyaluronic acid is an accurate predictor of mortality and morbidity over an 18-month period in patients treated by CAPD. Large quantities of hyaluronic acid are excreted in peritoneal dialysate, which in part represents local hyaluronic acid production.


Subject(s)
Hyaluronic Acid/blood , Hyaluronic Acid/urine , Peritoneal Dialysis, Continuous Ambulatory , Adult , Aged , Female , Humans , Hyaluronic Acid/metabolism , Kidney Failure, Chronic/epidemiology , Kidney Failure, Chronic/metabolism , Kidney Failure, Chronic/mortality , Male , Middle Aged , Molecular Weight , Morbidity , Peritoneum/metabolism , Prospective Studies , Survival Analysis
18.
Clin Sci (Lond) ; 82(2): 119-26, 1992 Feb.
Article in English | MEDLINE | ID: mdl-1311648

ABSTRACT

1. In experimental studies, activation of renal sympathetic nerves attenuates the natriuretic response to atrial natriuretic factor. We therefore investigated the response to low-dose infusion of atrial natriuretic factor in renal transplant recipients. 2. Eight male cyclosporin-treated renal transplant recipients received human-alpha atrial natriuretic factor (1-28) at a dose of 1.2 pmol min-1 kg-1 or placebo for 2 h in a placebo-controlled, randomized, cross-over study. The plasma atrial natriuretic factor concentration rose from 18.5 to 49.2 pmol/l in association with an immediate natriuresis (a rise of 49.1 mumol/min in the first 30 min, P less than 0.05; peaking at a 61% increase from baseline, P less than 0.01), diuresis (from 3.37 to 7.46 ml/min) and a threefold rise in urinary cyclic GMP excretion. 3. In response to infusion of atrial natriuretic factor, the packed cell volume rose by 4.2% (P less than 0.001) and the filtration fraction by 5% (from 22 to 27%, P less than 0.05), but there was no significant change in renal plasma flow, glomerular filtration rate or mean arterial blood pressure. Likewise, the plasma catecholamine concentrations, plasma renin activity and serum erythropoietin concentration remained unchanged. 4. The sensitivity of the renal allograft to plasma atrial natriuretic factor concentrations in the high physiological range suggests a role for endogenous atrial natriuretic factor in the modulation of graft function. Furthermore, the immediate natriuretic response to atrial natriuretic factor in the effectively denervated transplant kidney, in contrast to the delayed response seen in normal subjects, may imply that sympathetic nerves have an inhibitory effect on the renal response to atrial natriuretic factor in normal man.(ABSTRACT TRUNCATED AT 250 WORDS)


Subject(s)
Atrial Natriuretic Factor/physiology , Diuresis/physiology , Kidney Transplantation/physiology , Kidney/physiopathology , Albuminuria/physiopathology , Atrial Natriuretic Factor/blood , Cyclic GMP/urine , Erythropoietin/blood , Hematocrit , Hemodynamics/physiology , Humans , Kidney/blood supply , Kidney/innervation , Male , Middle Aged , Random Allocation
19.
Br J Clin Pract ; 46(4): 268-9, 1992.
Article in English | MEDLINE | ID: mdl-1290739

ABSTRACT

Wegener's granulomatosis is a form of systemic vasculitis. Untreated, it has a 90% two year mortality, but complete remission can be obtained in 93% of patients following treatment with cyclophosphamide (usually in combination with steroids). There is early and major involvement of the respiratory tract. Renal involvement adversely affects prognosis.


Subject(s)
Granulomatosis with Polyangiitis/complications , Infarction/etiology , Tongue/blood supply , Acute Kidney Injury/etiology , Female , Humans , Middle Aged
SELECTION OF CITATIONS
SEARCH DETAIL
...