Role of the family physician in controlling the epidemic of chronic kidney disease.

The term chronic kidney disease (CKD) signifies permanent reduction in renal function. It consists of 5 stages of increasing severity. CKD replaces the multiple terms like chronic renal failure in vogue earlier. The prevalence of CKD is rapidly increasing in the community and causing a huge burden on the community. Since the current marker of renal function-serum creatinine is not sensitive enough, measurement of estimated glomerular filtration rate (eGFR) has been proposed to quantify the renal function better. The family physician has a vital role to play in preventing the onset and progression of CKD. Prevention starts with maintaining a healthy lifestyle. The groups at risk for developing CKD like diabetics and hypertensives should be effectively treated. Yearly estimation of albuminuria (or microalbuminuria) and estimated GFR should be done. Optimal use of renoprotective drugs can delay the inevitable progression of CKD to end-stage renal disease (ESRD). The family physician is the key person, who can implement these measures at the primary care level. Referral to a nephrologist can be made once initially when the serum creatinine >2 mg% to establish the primary diagnosis; and subsequently the patient can be managed in consultation with the nephrologist. Only such an Integrated approach with the active participation of the family physician can successfully stem the upsurge in the tide of CKD.

Antibiotic resistance pattern among the Salmonella isolated from human, animal and meat in India.

The present study was conducted to study the antibiotic resistance pattern among nontyphoidal Salmonella isolated from human, animal and meat. A total of 37 Salmonella strains isolated from clinical cases (human and animal) and meat during 2008-2009 belonging to 12 serovars were screened for their antimicrobial resistance pattern using 25 antimicrobial agents falling under 12 different antibiotic classes. All the Salmonella isolates tested showed multiple drug resistance varying from 5.40% to 100% with 16 of the 25 antibiotics tested. None of the isolates were sensitive to erythromycin and metronidazole. Resistance was also observed against clindamycin (94.59%), ampicillin (86.49%), co-trimoxazole (48.65%), colistin (45.94%), nalidixic acid (35.10%), amoxyclave (18.90%), cephalexin, meropenem, tobramycin, nitrofurantoin, tetracycline, amoxicillin (8.10% each), sparfloxacin and streptomycin (5.40% each). Isolates from clinical cases of animals were resistant to as many as 16 antibiotics, whereas isolates from human clinical cases and meat were resistant to 9 and 14 antibiotics, respectively. Overall, 19 resistotypes were recorded. Analysis of multiple antibiotic resistance index (MARI) indicated that clinical isolates from animals had higher MARI (0.25) as compared to isolates from food (0.22) and human (0.21). Among the different serotypes studied for antibiogram, Paratyhi B isolates, showed resistance to three to 13 antibiotics, whereas Typhimurium strains were resistant to four to seven antibiotics. Widespread multidrug resistance among the isolates from human, animal and meat was observed. Some of the uncommon serotypes exhibited higher resistance rate. Considerable changes in the resistance pattern were also noted. An interesting finding was the reemergence of sensitivity to some of the old antibiotics (chloromphenicol, tetracycline).

Rhabdomyolysis, acute kidney injury and transverse myelitis due to naive heroin exposure.

Heroin exposure can cause various complications like seizures, stroke, spongiform encephalopathy, transverse myelopathy, plexopathy, compartment syndrome, rhabdomyolysis and renal failure due to various mechanisms. We report here a young male who smoked heroin for the first time and developed transverse myelitis, rhabdomyolysis and acute kidney injury requiring dialysis. His renal recovery was complete by four weeks, while neurological improvement occurred 8 to 12 weeks later. This case suggests a common pathogenic mechanism of heroin intoxication involving multiple systems of the body.

Diarrhea-related hemolytic uremic syndrome: unmasking antifactor H antibodies.

The cases of hemolytic uremic syndrome (HUS) preceeded by diarrhea are commonly labeled as D+ HUS. However, with severe renal failure or with delayed recovery, such cases should be evaluated for rarer associations like Factor H (FH), I and CD 46 deficiency or mutations. We report such a presentation of a young boy who initially came with diarrhea and had features of HUS with delayed renal recovery. He later turned out to have anti-FH antibody-related HUS.

Clinical approach to rapidly progressive renal failure.

Rapidly progressive renal failure (RPRF) is an initial clinical diagnosis in patients who present with progressive renal impairment of short duration. The underlying etiology may be a primary renal disease or a systemic disorder. Important differential diagnoses include vasculitis (systemic or renal-limited), systemic lupus erythematosus, multiple myeloma, thrombotic microangiopathy and acute interstitial nephritis. Good history taking, clinical examination and relevant investigations including serology and ultimately kidney biopsy are helpful in clinching the diagnosis. Early definitive diagnosis of RPRF is essential to reverse the otherwise relentless progression to end-stage kidney disease.

Endothelial function and oxidative stress in chronic kidney disease of varying severity and the effect of acute hemodialysis.

AIM: Oxidative stress (OS) and endothelial dysfunction are implicated in accelerated atherosclerosis in chronic kidney disease (CKD). We assessed endothelial function, OS, and carotid intimal medial thickness (CIMT) and their correlates in 44 CKD stage 5 patients (group III) before and after hemodialysis (HD), 40 patients of CKD stages 3 and 4 (group II), and 25 matched controls (group I). METHODS: OS was measured by serum concentration of antioxidants; vitamin C and fractional reducing ability of plasma (FRAP) and pro-oxidant; thiobarbituric acid reactive substances (TBARS). Ultrasonography of carotid artery for CIMT and of brachial artery for flow-mediated dilatation (endothelium-dependent dilatation, EDD) was done. RESULTS: TBARS increased significantly with severity of CKD. Antioxidants FRAP and vitamin C were significantly lower in CKD patients as compared with controls, but there was no significant difference between groups II and III. EDD decreased significantly with severity of CKD, whereas CIMT though higher in CKD patients as compared with controls was not significantly different between groups II and III. After a session of HD as compared with predialysis, levels of TBARS decreased, whereas those of FRAP, vitamin C, and EDD increased. On multivariate analysis, there was negative correlation of TBARS with glomerular filtration rate (GFR), serum albumin, hemoglobin, and EDD. Vitamin C had positive correlations with GFR, serum albumin, hemoglobin, and EDD. EDD had direct correlation with GFR, whereas CIMT correlated negatively with EDD. CONCLUSIONS: Endothelial dysfunction and OS occur early in CKD, are closely related to each other and structural atherosclerosis, and are proportional to decline in GFR.

Transient IgA nephropathy with acute kidney injury in a patient with dengue fever.

Dengue virus infection can clinically manifest as dengue fever, dengue shock syndrome and dengue hemorrhagic fever. Acute kidney injury as a result of dengue virus infection can occur due to various reasons including hypotension, rhabdomyolysis, sepsis and rarely immune complex mediated glomerular injury. However, glomerulonephritis associated with IgA Nephropathy in dengue virus infection has not been reported previously. We report a case of 15-year-old boy who was admitted with dengue fever and dialysis dependant acute kidney injury. Urine examination showed microscopic glomerular hematuria and proteinuria. Kidney biopsy showed mesangial proliferation with mesangial IgA dominant immune complex deposits and acute tubular necrosis. A repeated kidney biopsy 6 weeks after clinical recovery showed reversal of glomerular changes as well as resolution of mesangial IgA deposits.

Renal involvement in leprosy: report of progression from diffuse proliferative to crescentic glomerulonephritis.

Renal involvement in leprosy has been reported rarely in the literature. Acute kidney injury in patients with leprosy is uncommon and may occur due to acute tubular necrosis, drug-induced interstitial nephritis and rarely crescentic glomerulonephritis. The latter with histologic confirmation of the diagnosis has been reported in very few cases of leprosy. A 25-year-old male, on therapy for multibacillary leprosy, was found to have deranged renal functions on evaluation for a history of nausea, vomiting, swelling and episode of haematuria. Kidney biopsy was performed twice over a period of 2 weeks, showing progression from diffuse proliferative glomerulonephritis to crescentic glomerulonephritis, pauci-immune in nature. The patient was treated aggressively with intravenous steroids, following which his renal functions stabilized. Crescentic glomerulonephritis, an extremely rare phenomenon in leprosy, should be considered in these patients presenting with features of acute kidney injury. Timely performed renal biopsy assists in accurate diagnosis and appropriate management of the patient, hence preserving renal parenchyma. Rapid progression from diffuse proliferative glomerulonephritis to crescentic glomerulonephritis in a patient with leprosy is described herein for the first time in the literature.

Membranous glomerulonephritis in a patient with ankylosing spondylitis: a rare association.

Ankylosing spondylitis is a chronic inflammatory disease of the vertebral joints and soft tissues. Renal involvement, apart from amyloidosis, is rare in this disorder. Of the various glomerulonephritides reported in association with ankylosing spondylitis, IgA nephropathy is the most common. Membranous glomerulonephritis occurs very rarely in patients with ankylosing spondylitis, and only four such cases have been reported in the available English literature. Due to the rarity of this association, membranous glomerulonephritis may not initially be considered in patients with ankylosing spondylitis and proteinuria. We report the case of a 29-year-old man with ankylosing spondylitis who presented with pedal edema and was detected to have nephrotic syndrome. A percutaneous renal biopsy showed features of membranous glomerulonephritis with capillary wall granular deposits of IgG and C3 on immunofluorescence and subepithelial immune complex deposits on electron microscopy. No other secondary cause of membranous glomerulopathy was found on extensive investigations. Membranous glomerulonephritis is extremely rare in association with ankylosing spondylitis, the present case being the fifth such report. The exact relationship of these two entities (etiological or coincidental) still needs to be elucidated. The occurrence of this rare association needs to be recognized and differentiated from other more common causes of renal involvement in ankylosing spondylitis.