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Renal AND Proteinuria [keywords]
- Post-infectious glomerulonephritis presenting as acute renal failure in a patient with Lyme disease. [Journal Article]
- J Renal Inj Prev 2014; 3(1):17-20.
We report a case of a patient with acute renal failure in Lyme disease-associated focal proliferative mesangial nephropathy. Lyme disease is a vector-borne disease caused by Borrelia burgdorferi, transmitted by the bite of an infected ixodes tick. Post-infectious glomerulonephritis (GN)secondary to Borrelia burgdorferi infection in man could be fatal, as it is in canine Lyme borreliosis.A 61-year old man with chronic ethanolic hepatitis was admitted to a provincial hospital, complaining of nausea, diarrhoea and loss of his sense of taste. A few days prior hospitalization, he had been bitten by a tick. He developed erythema gyratum repens in the right leg, thorax and face. Kidney function was altered despite normal urine flow: creatinine 5.04 mg/dl and BUN 126 mg/dl. Urinalysis showed light proteinuria and microscopic hematuria. IgG and IgM antibodies to Borrelia burgdorferi were detected by ELISA and Western blot confirmed the diagnosis. Renal biopsy showed mild mesangial proliferation and mesangial and paramesangial deposits on AFOG stain. A diagnosis of acute renal failure in Lyme disease-associated focal proliferative IgA nephropathy was made. Intravenous antibiotic medication was started (ceftriaxone 1 gram daily i.v.). The patient was later discharged, serum creatinine had decreased to 3.5 mg/dl with a BUN of 58 mg/dl, and a slight improvement was observed on follow-up.Borrelia burgdorferi is a possible cause of post-infectious GN in humans as it is in dogs. Difficulties in identifying Borrelia burgdorferi may also be one of the reasons for the paucity of reports on the association of this infection with glomerulonephritis in humans. Currently, various types of histological renal lesions have been reported.
- Amyloid A amyloidosis with subcutaneous drug abuse. [Journal Article]
- J Renal Inj Prev 2014; 3(1):11-6.
Amyloid A (AA) amyloidosis is a systemic form of amyloidosis secondary to chronic infections and inflammatory disorders. An acute-phase protein produced by the liver, serum amyloid A (SAA) is the precursor of AA amyloid fibrils. AA amyloid deposition occurs predominantly in the kidneys, spleen, adrenal glands, liver and gastrointestinal tract. The manifestations of AA amyloidosis involving the kidneys include proteinuria, tubular dysfunction and progressive loss of renal function.We report a 47-year-old drug addict who developed AA amyloidosis as a result of recurrent suppurative skin infections secondary to subcutaneous drug injection. Elevated C-reactive protein concentrations attested to the presence of a chronic systemic inflammatory state. He suffered from the nephrotic syndrome and insidious loss of renal function. Isosthenuria and glycosuria were indicative of renal tubular dysfunction. Renal biopsy demonstrated AA amyloidosis involving the glomeruli, tubular basement membranes and blood vessel walls.Superimposed acute tubular necrosis due to concomitant endocarditis and cocaine use accelerated his renal disease. CASE presentation is followed by a brief discussion of clinical features, natural history and outcome of AA amyloidosis with a particular emphasis on AA amyloidosis as a complication of subcutaneous drug abuse.
- IgM nephropathy: timely response to a call for action. [Journal Article]
- J Renal Inj Prev 2014; 3(1):5-6.
Immunoglobulin M (IgM) is the largest antibody molecule and is deposited in the glomeruli in a wide variety of both primary and secondary glomerulopathies. The data on its pathogenic role are conflicting till date. A recent study provides evidence for the involvement of natural antibody IgM in fixing and activating complement and causing glomerular injury, proteinuria, and glomerulosclerosis in an animal model. This finding is important in understanding the pathogenesis of the related disorder of IgM nephropathy.
- RENIN ANGIOTENSIN SYSTEM WITHIN THE DIABETIC PODOCYTE. [JOURNAL ARTICLE]
- Am J Physiol Renal Physiol 2014 Oct 22.
Diabetic kidney disease is the leading cause of end-stage renal disease. Podocytes are differentiated cells necessary for the development and maintenance of the glomerular basement membrane and the capillary tufts, as well as the function of the glomerular filtration barrier. The epithelial glomerular cells express a local renin angiotensin system (RAS), that varies in different pathological situations such as hyperglycemia or mechanical stress. RAS components have been shown to be altered in the diabetic podocytopathy, and their modulation may modify diabetic nephropathy progression. Podocytes are a direct target for angiotensin II - mediated injury by altered expression and distribution of podocyte proteins. Furthermore, angiotensin II promotes podocyte injury indirectly by inducing cellular hypertrophy, increased apoptosis, and changes in the anionic charge of glomerular basement membrane, among other effects. RAS blockade has been shown to decrease the level of proteinuria and delay the progression of chronic kidney disease. This review summarizes the local intraglomerular RAS and its imbalance in diabetic podocytopathy. A better understanding of the intrapodocyte RAS might provide a new approach for diabetic kidney disease treatment.
- Cardiovascular disease and its relationship with chronic kidney disease. [Journal Article]
- Eur Rev Med Pharmacol Sci 2014 Oct; 18(19):2918-26.
Cardiovascular disease (CVD), the leading cause of death, is mostly precipitated by cardiometabolic risk and chronic kidney disease (CKD). CVD and kidney disease are closely interrelated and disease of one organ cause dysfunction of the other, ultimately leading to the failure of both organs. Patients with end-stage renal disease (ESRD) are at much higher risk of mortality due to CVD. Traditional CVD risk factors viz., hypertension, hyperlipidemia, and diabetes do not account for the high cardiovascular risk in CKD patients and also standard clinical interventions for managing CVD that are successful in the general population, are ineffective to lower the death rate in CKD patients. Nontraditional factors, related to disturbed mineral and vitamin D metabolism were able to provide some explanation in terms of vascular calcification, for the increased risk of CVD in CKD. Fibroblast Growth Factor 23, a bone-derived hormone that regulates vitamin D synthesis in renal proximal tubules and renal phosphate reabsorption, has been suggested to be the missing link between CKD and CVD. Acute Kidney Injury (AKI) is strongly related to the progress of CVD and its early diagnosis and treatment has significant positive effect on the outcomes of CVD in the affected patients. Besides this, non-dialysable protein-bound uraemic toxins such as indoxyl sulfate and p-cresyl sulfate, produced by colonic microbes from dietary amino acids, appear to cause renal dysfunction. Thus, therapeutic approaches targeting colonic microbiota, have led to new prospects in early intervention for CKD patients. Intervention targets for preventing CVD events in CKD patients ideally should include control of blood pressure and dyslipidemia, diabetes mellitus, lowering proteinuria, correction of anemia, management of mineral metabolism abnormalities and life style changes including smoking cessation, decreased consumption of salt, and achievement of normal body mass index. Use of β-blockers, renin-angiotensin blockers, diuretics, statins, and aspirin are helpful in the early stages of CKD. In this review, we will address the biological, pathological and clinical relationship between CVD and CKD and their therapeutic management.
- Astragalus (a traditional Chinese medicine) for treating chronic kidney disease. [JOURNAL ARTICLE]
- Cochrane Database Syst Rev 2014 Oct 22.:CD008369.
Astragalus (Radix Astragali, huang qi) is the dried root of Astragalus membranaceus (Fisch.) Bge. var. mongholicus (Bge.) Hsiao or Astragalus membranaceus (Fisch.) Bge. (Family Leguminosae). It is one of the most widely used herbs in traditional Chinese medicine for treating kidney diseases. Evidence is needed to help clinicians and patients make judgments about its use for managing chronic kidney disease (CKD).This review evaluated the benefits and potential harms of Astragalus for the treatment of people with CKD.We searched the Cochrane Renal Group's Specialised Register to 10 July 2014 through contact with the Trials' Search Co-ordinator using search terms relevant to this review. We also searched CINAHL, AMED, Current Controlled Trials, OpenSIGLE, and Chinese databases including CBM, CMCC, TCMLARS, Chinese Dissertation Database, CMAC and Index to Chinese Periodical Literature.Randomised controlled trials (RCTs) and quasi-RCTs comparing Astragalus, used alone as a crude herb or an extract, with placebo, no treatment, or conventional interventions were eligible for inclusion.Two authors independently extracted data and assessed risk of bias in the included studies. Meta-analyses were performed using relative risk (RR) for dichotomous outcomes and mean differences (MD) for continuous outcomes, with 95% confidence intervals (CI).We included 22 studies that involved 1323 participants, of whom 241 were receiving dialysis treatment. Risk of bias was assessed as high in six studies, and unclear in the remaining 16 studies. Study quality was low overall.Our nominated primary outcomes of time to requirement for renal replacement therapy (RRT) or initiation of dialysis and all-cause mortality were not reported in any of the included studies.Results concerning the effects of Astragalus on kidney function were inconsistent. Astragalus significantly increased CrCl at end of treatment (4 studies, 306 participants: MD 5.75 mL/min, 95% CI 3.16 to 8.34; I² = 0%), decreased SCr (13 studies, 775 participants: MD -21.39 µmol/L, 95% CI -34.78 to -8; I² = 70%) and especially in those whose baseline SCr was < 133 µmol/L in particular (3 studies, 187 participants: MD -2.52 µmol/l, 95% CI -8.47 to 3.42; I² = 0%). Astragalus significantly decreased 24 hour proteinuria at end of treatment (10 studies, 640 participants; MD -0.53 g/24 h, 95% CI -0.79 to -0.26; I² = 90%); significantly increased haemoglobin levels overall (4 studies, 222 participants): MD 9.51 g/L, 95% CI 4.90 to 14.11; I² = 0%) and in haemodialysis patients in particular (3 studies, 142 participants: MD 11.20 g/L, 95% CI 5.81 to 16.59; I² = 0%). Astragalus significantly increased serum albumin (9 studies, 522 participants: MD 3.55 g/L, 95% CI 2.33 to 4.78; I² = 65%). This significant increase was seen in both dialysis (3 studies, 152 participants): MD 4.04 g/L, 95% CI 1.91 to 6.16; I² = 72%) and non-dialysis patients (6 studies, 370 participants: MD 3.24 g/L, 95% CI 1.70 to 4.77; I² = 61%). Astragalus significantly decreased systolic blood pressure (2 studies, 77 participants: MD -16.65 mm Hg, 95% CI -28.83 to -4.47; I² = 50%), and diastolic blood pressure (2 studies, 77 participants: MD -6.02 mm Hg, 95% CI -10.59 to -1.46; I² = 0%).Six of 22 included studies reported no adverse effects were observed; while the remaining 16 studies did not report adverse effects.Although Astragalus as an adjunctive treatment to conventional therapies was found to offer some promising effects in reducing proteinuria and increasing haemoglobin and serum albumin, suboptimal methodological quality and poor reporting meant that definitive conclusions could not be made based on available evidence.
- Pure Motor Axonal Neuropathy, Organomegaly, Impaired Glucose Tolerance, M Protein, Skin Changes, Multiple Plasmacytomas & Acute Interstitial Nephritis in Osteolytic Myeloma: Beyond POEMS! [Journal Article]
- Indian J Hematol Blood Transfus 2014 Sep; 30(Suppl 1):115-9.
The authors describe a case of 52-year-old male who presented with sudden onset deterioration of weakness of both lower limbs and retention of urine. He had 1 month history of gradually progressive weakness of legs. On examination, there were lower motor neuron signs in lower extremity, digital clubbing and a lump over left iliac fossa. Routine blood tests showed impaired glucose tolerance, confirmed by oral glucose tolerance test while renal parameters were normal. Magnetic resonance imaging of spine documented osteolytic lesions, long segment epidural mass in thoracic spine and a mass overlying the left iliac bone, both were revealed to be plasmacytoma following cytology. Ultrasonography of abdomen showed splenomegaly. Nerve conduction studies showed gross axonal, motor, asymmetric polyneuropathy with conduction block involving all the four extremities, mainly lower limbs with sensory sparing. Serum protein electrophoresis showed M spike, and bone marrow showed diffuse neoplastic plasma cell proliferation. Osteolytic lesion was present in skull radiograph. Then in the course of illness the patient developed acute renal failure due to acute interstitial nephritis as evidenced from proteinuria and kidney biopsy, which improved with steroids and chemotherapy but unfortunately we lost the patient after 2 weeks of initiation of chemotherapy.
- [Hereditary fibrinogen Aα-chain amyloidosis caused by the E526V mutation: a case report and literature review]. [English Abstract, Journal Article]
- Beijing Da Xue Xue Bao 2014 Oct 18; 46(5):802-4.
Mutations in the fibrinogen Aα-chain genes are the most common cause of hereditary renal amyloidosis. The renal histologic appearance in the patient is characteristic and shows striking glomerular enlargement with almost complete obliteration of the normal glomerular architecture by extensive amyloid deposition. In contrast, the vessels and renal tubular interstitium of such patient contains almost no amyloid at all. Here, we described a patient with hereditary fibrinogen amyloidosis, who presented with proteinuria, hypertension and renal failure. He was shown to be heterozygous for the relevant mutation encoding the E526V fibrinogen variant.
- Intensification of blood pressure treatment in Pasifika people with type 2 diabetes and renal disease: a cohort study in primary care. [Journal Article]
- N Z Med J 2014; 127(1404):17-26.
Chronic kidney disease is common in Pasifika people with type 2 diabetes. Lowering blood pressure (BP) and reducing proteinuria may slow the rate of progression of renal disease.We conducted a 2-year study in patients with type 2 diabetes with estimated glomerular filtration rate (eGFR) greater than or equal to 40ml/mmin/1.73m2 and urinary albumin-creatinine ratio (ACR) greater than or equal to 40 mg/mmol to evaluate a community-based programme aimed at optimising BP. Primary outcomes included BP reduction, remission of albuminuria and change in eGFR.Thirty-nine of 47 patients completed greater than or equal to 17 months of intervention. The mean age was 53 plus or minus 8 years; 77% were male. An increase in antihypertensive therapy intensity was accompanied by a median (IQR) reduction in BP of 13[-1.5-22.5)/ 12(1-19) mmHg p<0.05] and urinary ACR (51(20-97) vs. 126(65-194) mg/mmol, p<0.05). Twelve (28%) of 43 patients achieving remission of albuminuria had a faster eGFR loss in the first year compared to the non-remitting group [13.6(4.0-16.6) vs. 3.5(-0.97-7.5) ml/min/1.73m2/year, (p=0.02), but the rate of loss slowed in the second year. Two patients reached ESRF.This community-based programme was effective in lowering BP and urinary ACR. In patients who achieved remission of albuminuria, a slower eGFR decline was observed after 12 months.
- Survival after acute kidney injury requiring dialysis: Long-term follow up. [Journal Article]
- Hemodial Int 2014 Oct.:S1-6.
Data on long-term follow up after acute kidney injury (AKI) requiring dialysis are scarce. The aim of this study was to describe and identify factors associated with survival, recovery of kidney function at discharge, and long-term follow up of renal function in AKI patients requiring dialysis. All AKI patients requiring dialysis during calendar year 2000-2011 treated with conventional hemodialysis and daily shift continuous venovenous hemodialysis (8-hour 40 L dialysate) were included. The data were mean and SD. The results were: 65.8% male; 33.9% diabetic; 75% dipstick positive proteinuria on admission; 72.5% medical AKI; and 27.6% surgical AKI of those (14.2%) who had postcardiovascular surgery. At discharge mortality by cause of AKI: medical 25%, surgical 29.8%; and at the end of study: medical 35.3%, surgical 43.6%. Two-hundred thirty-four patients were discharged alive (mortality 26%). Forty-two died after discharge; 50% in the first 156 days post discharge. Mortality at the end of study was 37.8%. Follow-up (F/U) (1-86 m). At discharge, 200 recovered from kidney function (63.2%), and of those who died in the hospital 80.5% did not recover from kidney function (died dialysis dependent). Baseline serum creatinine was 1.33 mg/dL (0.64), estimated glomerular filtration rate (eGFR) 63.4 mL/minute (29.3), peak creatinine 6.3 mg/dL (2.9), and peak blood urea nitrogen 88.1 mg/dL (39.9). At discharge, serum creatinine was 3.1 mg/dL (2.1) and eGFR was 31.6 mL/minute (27.4); at 6 months, creatinine was 1.66 mg/dL (1.1) and eGFR was 60.8(36); at all F/U times, the creatinine was higher and eGFR was lower than the baseline values (P < 0.05). Of the nonsurvivors, the only significant difference was a lower albumin at baseline (2.9 vs. 3.1 g/dL) (P < 0.05) and lower peak creatinine (5.5 vs. 6.8 mg/dL) (P < 0.05). The mean survival time was 45.4 months. The survival of the patients who recovered from kidney function at discharge was longer than the ones who did not recover (59.7 vs. 16 m, P < 0.05). By Cox regression, the factors significant for survival were peak creatinine and status at discharge. During follow up (data up to 54 months), the percentage of patients with eGFR < 60 mL/minute decreased from 90.9% at discharge to 63.6% at 24 months, then increased to 81.8% at 30 months and longer. The percentage of patients with eGFR < 30 mL/minute decreased from 45.4% at discharge to 18.2% at 24 months to increase at a later date (27-36%). The percentage of patients with eGFR < 15 mL/minute decreased from 45.45% at discharge to 18% until 24 months of follow up (to increase to 27.7% at later dates). AKI requiring dialysis has a significant effect on GFR with almost 80% of the survivors having chronic kidney disease stage 3 or worse. Furthermore, progression was observed on the long-term follow up. Factors affecting the survival included peak creatinine and status of recovery of kidney function at discharge.