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Biomedical subjects

K S Ratnakar

Publications and source records attributed to K S Ratnakar.

At least 19 recordsLinked to original sources

Lymph node infarction--a rare complication associated with disseminated intra vascular coagulation in a case of dengue fever.

BACKGROUND: Lymph node infarction is known to occur in association with many non-neoplastic and neoplastic conditions however its occurrence in association with DIC is not reported hitherto in the literature. CASE PRESENTATION: We describe an unusual case of lymph node infarction in a twenty seven year old male following disseminated intravascular coagulation (DIC) in a case of dengue fever. Multiple sections of the infarcted and the surrounding non-infarcted lymph nodes failed to reveal any predisposing condition. How ever the parahilar vessels showed thrombotic occlusion, which must have been responsible for the infarction. CONCLUSION: Global infarction of the lymph node may mask the underlying pathology. Any malignancy especially lymphoma may coexist or follow lymph node infarction, therefore the patient needs constant surveillance.

Journal Article↗

Multicystic renal dysplasia.

Multicystic renal dysplasia, the most common form of cystic renal disease in the newborn period, is a clinically important consequence of abnormal nephrogenesis. It usually presents as an abdominal mass. The dysplasias are usually unilateral, but it can be bilateral, segmental or focal. The clinical presentation usually depends on the extent of the dysplastic involvement and the degree of the associated urinary obstruction. Here, we present a case of histologically multicystic renal dysplasia, which is ?bilateral. The left kidney showed typical radiological, gross and histopathological features of multicystic dysplasia, but the right kidney showed only radiological features of dysplastic cystic kidney.

Diagnosis, Differential↗

Carvedilol: a beta blocker with antioxidant property protects against gentamicin-induced nephrotoxicity in rats.

Gentamicin is an antibiotic effective against gram negative infections, whose clinical use is limited by its nephrotoxicity. Since the pathogenesis of gentamicin-induced nephrotoxicity involves oxygen free radicals, the antioxidant carvedilol may protect against gentamicin-induced renal toxicity. We therefore tested this hypothesis using a rat model of gentamicin nephrotoxicity. Carvedilol (2 mg/kg) was administered intraperitoneally 3 days before and 8 days concurrently with gentamicin (80 mg/kg BW). Estimations of urine creatinine, glucose, blood urea, serum creatinine, plasma and kidney tissue malondialdehyde (MDA) were carried out, after the last dose of gentamicin. Kidneys were also examined for morphological changes. Gentamicin caused marked nephrotoxicity as evidenced by increase in blood urea, serum creatinine and decreased in creatinine clearance. Blood urea and serum creatinine was increased by 883% and 480% respectively with gentamicin compared to control. Carvedilol protected the rats from gentamicin induced nephrotoxicity. Rise in blood urea, serum creatinine and decrease in creatinine clearance was significantly prevented by carvedilol. There was 190% and 377% rise in plasma and kidney tissue MDA with gentamicin. Carvedilol prevented the gentamicin induced rise in both plasma and kidney tissue MDA. Kidney from gentamicin treated rats, histologically showed necrosis and desquamation of tubular epithelial cells in renal cortex, whereas it was very much comparable to control with carvedilol. In conclusion, carvedilol with its antioxidant property protected the rats from gentamicin-induced nephrotoxicity.

Adrenergic beta-Antagonists↗

Ginkgo biloba extract ameliorates gentamicin-induced nephrotoxicity in rats.

The effect of Ginkgo biloba (EGb), a plant extract with an antioxidant effect, has been studied on gentamicin-induced nephrotoxicity in male wistar rats. Ginkgo biloba extract (300 mg/kg BW) was administered orally 2 days before and 8 days concurrently with gentamicin (80 mg/kg BW). Saline treated animals served as control. Estimations of urine creatinine, glucose, blood urea, serum creatinine, plasma and kidney tissue MDA were carried out after 8 days of gentamicin treatment. Kidneys were examined using histological techniques. Blood urea and serum creatinine were increased by 896% and 461% respectively, with gentamicin, compared to saline treated group. Creatinine clearance was significantly decreased with gentamicin. Ginkgo biloba extract protected rats from gentamicin-induced nephrotoxicity. Changes in blood urea, serum creatinine and creatinine clearance induced by gentamicin were significantly prevented by Ginkgo biloba extract. There was a 177% and 374% rise in plasma and kidney tissue MDA with gentamicin, which were significantly reduced to normal with Ginkgo biloba extract. Histomorphology showed necrosis and desquamation of tubular epithelial cells in renal cortex with gentamicin, while it was normal and comparable to control with Ginkgo biloba extract. These data suggest that supplementation of Ginkgo biloba extract may be helpful to reduce gentamicin nephrotoxicity.

Administration, Oral↗

Melatonin, a pineal hormone with antioxidant property, protects against gentamicin-induced nephrotoxicity in rats.

The present study investigated the effects of melatonin, an antioxidant, on gentamicin-induced nephrotoxicity in rats. Melatonin (5 mg/kg p.o.) was used 3 days before and 8 days simultaneously with gentamicin (80 mg/kg i.p.) Saline-treated animals served as controls. Determinations of urinary creatinine, N-acetyl-beta-D-glucosaminidase, glucose, protein, blood urea, serum creatinine, plasma and kidney tissue malondialdehyde (MDA), and antioxidant enzyme levels in kidney tissue were done after 8 days of gentamicin treatment. The kidneys were also examined for morphological changes using histological techniques. Gentamicin caused nephrotoxicity as evidenced by marked elevation in blood urea and serum creatinine. Mean blood urea and serum creatinine levels were 289+/-50, and 2.5+/-0.5 mg/dl, respectively, in rats treated with gentamicin. Melatonin significantly protected the rats from gentamicin-induced nephrotoxicity; blood urea and serum creatinine levels were 23+/-2.7 and 0.88+/-0.19 mg/dl, respectively. The creatinine clearance was decreased with gentamicin treatment (0.048+/- 0.007 ml/min) as compared with controls (0.41+/-0.08 ml/h/kg). In rats treated with melatonin plus gentamicin, the creatinine clearance was similar to controls (0.41+/-0.08 ml/h/kg). The product of lipid peroxidation (MDA) was markedly increased in plasma (2.10+/-0.15 nmol) and kidney tissue (8.87+/-3.2 nmol/mg protein) with gentamicin treatment. Melatonin prevented the gentamicin-induced rise in plasma MDA (1.03+/-0.27 nmol) and kidney tissue MDA (2.57+/-0.87 nmol/mg protein). An increased excretion of urinary N-acetyl-beta-D-glucosaminidase, glucose, and protein by gentamicin was also prevented by melatonin. Kidneys from gentamicin-treated rats showed tubular epithelial loss with intense granular degeneration involving more than 50% of renal cortex, while there were findings comparable to controls in melatonin plus gentamicin treated rats. The present study indicates that melatonin significantly protects against gentamicin-induced renal toxicity in Wistar rats.

Animals↗

Effect of pentoxifylline on cyclosporine-induced nephrotoxicity in rats.

Effect of unique hemorrheologic agent pentoxifylline (PTX) was investigated on cyclosporine (CsA) induced nephrotoxicity in rats. Compared to saline control, CsA produced significant increase in blood urea and serum creatinine. Pentoxifylline treatment prevented the CsA-induced rise in blood urea and serum creatinine. Creatinine clearance (Ccr) and lithium clearance (Licr) was decreased with CsA. PTX treatment prevented the CsA-induced decrease in Ccr and Licr. Malondialdehyde (MDA) was increased with CsA compared to saline treated animals. PTX prevented the CsA-induced MDA rise. Kidney form CsA treated rat showed marked vacuolar degeneration of tubular epithelium with excess of microcalcification. Severity of the lesions was markedly reduced in rats treated with PTX plus CsA. The results indicate that PTX reduces CsA-induced renal toxicity in rats.

Animals↗

Melatonin: an antioxidant protects against cyclosporine-induced nephrotoxicity.

BACKGROUND: Cyclosporine (CsA) causes a dose-related decrease in renal function in experimental animals. Different mediators for CsA nephrotoxicity have been suggested; oxygen free radicals are one of them. In experimental model of Wistar rats, the role of antioxidant melatonin (Mel), the main product of pineal secretion, was investigated in CsA nephrotoxicity. METHODS: Male Wistar rats were divided into four groups: saline control, 50 mg/kg CsA, 500 microg/kg Mel, and CsA + Mel. At the end of 14th day of treatment, blood urea, creatinine, malondialdehyde, and creatinine and lithium clearance were estimated. Histopathological examination of kidney from all the groups was performed. RESULTS: CsA caused marked elevation in blood urea, serum creatinine, and plasma malondialdehyde and a decrease in creatinine and lithium clearance. Mel significantly antagonized CsA-induced renal impairment. Microcalcification in corticomedullary junction seen with CsA was prevented by Mel. CONCLUSION: These results indicate that Mel, through its antioxidant properties, provides protection against CsA-induced nephrotoxicity.

Animals↗

Lacidipine protects against cyclosporine-induced nephrotoxicity in rats.

The effect of lacidipine (LA), a new calcium channel blocker with an antioxidant effect, has been studied on cyclosporine (CsA)-induced nephrotoxicity in male Wistar rats. Lacidipine (1 mg/kg BW) was administered orally 3 days before and 14 days concurrently with CsA (50 mg/kg BW orally). Urine volume, Na+, K+, Li+ and creatinine in urine, and blood urea, serum creatinine, lithium, plasma malondialdehyde (MDA) and CsA levels were estimated in blood after 14 days CsA treatment. Kidneys were examined using histological techniques. Blood urea and serum creatinine were increased by 305 and 211%, respectively, with CsA when compared to the saline-treated animals. Creatinine clearance (Ccr) and lithium clearance (Licr) were decreased and proximal tubule fractional reabsorption 1-(Licr/Ccr) was significantly increased with CsA. Lacidipine protected rats from CsA-induced nephrotoxicity. Changes in blood urea, serum creatinine, Ccr, Licr and proximal tubule fractional reabsorption induced by CsA were significantly prevented by LA. There was a 160% rise in MDA levels with CsA, which was significantly reduced equal to control with LA. Histomorphology showed microcalcification with CsA, while it was normal with LA. In rats treated with LA, CsA did not show any microcalcification. Our data suggest that supplementation of LA may be helpful to reduce CsA nephrotoxicity.

Animals↗

Cardioprotective effect of magnesium chloride in experimental acute myocardial infarction.

Cardioprotective role of intravenous administration of magnesium chloride was evaluated in rabbits by biochemical and histopathological parameters. Myocardial damage was induced by injecting (i.v.) isoprenaline 1, 2.5, 5 and 7.5 mg/kg body weight of animal. There was a dose dependent increase in the activity of cardiac enzyme creatinine kinase CK (C Max). Maximal elevation of CK (C Max) was observed with 2.5 mg isoprenaline. The mean T-max (mean of the time duration in hr at which maximum creatinine kinase activity of individual rabbit was observed in a group) shifted early, significantly with 2.5, 5 and 7.5 mg isoprenaline compared to control group. Histopathologically, myocardial damage was quite significant in 2.5 mg isoprenaline subgroup of animals. A mortality of 29% was observed in animals injected with 5 and 7.5 mg isoprenaline, whereas all animals subjected with 1 and 2.5 mg isoprenaline were alive for 72 hr. Considering the data on serial determination of cardiac enzyme CK and histopathological changes, 2.5 mg isoprenaline was chosen as standard dose to study efficacy of cardioprotection by gold standard verapamil and magnesium chloride. Verapamil (5 microM) injected prior to 2.5 mg isoprenaline administration revealed significant reduction of CK (C Max) activity (P < 0.05) compared to animals infused with isoprenaline alone. T-max value did not show any alteration in both the groups. Histopathological findings showed no areas of necrosis and cellular infiltrates in animals primed with 2.5 mg isoprenaline following verapamil. Highly significant reduction in CK (C-max) activity was observed in animals administered with 40 mg magnesium chloride prior to isoprenaline compared to animals treated with isoprenaline alone (P < 0.001). In addition to this, significant delay in T-max of CK activity was observed in group treated with 40 mg magnesium chloride and isoprenaline compared to group treated with only isoprenaline (P < 0.01). The study clearly highlighted and confirmed the valuable role of magnesium chloride as cardioprotective agent.

Animals↗

Clinicohistopathological findings of gelatinous droplike corneal dystrophy among Asians.

We describe the findings in nine Asian-Indian patients with gelatinous droplike corneal dystrophy (GDCD). Most patients showed initial signs of bilateral decreased vision and photophobia at an early age. The siblings were affected in four cases, and parental consanguinity was recorded in seven cases. We classified the disease into three forms based on clinicopathologic findings. Clinically, the mild form of the disease was evidence by central subepithelial, whitish-yellow, nodular lesions that corresponded to the subepithelial nodular deposits seen histologically. In the moderate form, the lesions coalesced, forming central, diffuse subepithelial lesions with superficial vascularization. On histology, the amyloid deposits assumed a sheetlike distribution in the subepithelial regions and in the superficial stroma. Aggregates of chronic inflammatory cells and stromal neovascularization were seen in the adjacent stroma. The severe form presented as diffuse, whitish opacification of the cornea with extensive neovascularization and scarring. Histologically this form was characterized by a visible plaque of vascularized scar tissue that partly replaced the stroma and enveloped the amyloid deposits. Frequent, early recurrence of the disease was noted in the grafts. This study provides a detailed clinicopathologic description of GDCD from the Indian subcontinent. We also discuss previously unreported findings from the most advanced stage of the disease.

Adolescent↗

Hemangioblastoma of the IV ventricle.

A case of solid hemangioblastoma in the IV ventricle in a 16-year-old boy is reported because of the rarity of this type of lesion. Microsurgical removal of the lesion was accomplished without any side effects in this highly vascular tumor in a strategic location.

Adolescent↗

Diagnostic dilemma of an intramedullary vascular malformation. A case report.

A young man was seen at a neurologic center for a slowly progressive myelopathy involving the lower limbs in 1983. After examination and investigations, a diagnosis of chronic tuberculous spinal arachnoiditis was made and the patient was administered antituberculous treatment. However, his condition continued to deteriorate. He was reviewed at another center in 1985, where a diagnosis of demyelinating disorder was made, for which he was treated. However, this also did not help, and he was diagnosed as having a nonspecific spinal arachnoiditis at yet another center in 1988. His condition continued to worsen, and after ten years of symptoms, when magnetic resonance imaging (MRI) was done, an intramedullary cystic lesion opposite D-12 vertebrae was seen, which on histopathology was proved to be a vascular malformation. After excision of the lesion his neurologic status has been slowly improving. The conditions that a malformation could mimic, misleading a clinician, and the role of MRI in clinching the diagnosis are highlighted.

Adult↗

Endobronchial metastasis from giant cell tumor of bone.

A young woman presented with cough, dyspnea on exertion, and weight loss. A chest roentgenogram revealed collapse of the left lung. On doing fiberoptic bronchoscopy, a growth was found in the left main bronchus. Cytologic examination and sections from cell block revealed that it was a metastatic growth from a giant cell tumor (GCT) of the bone. To the best of our knowledge, this is the first report of endobronchial metastasis from a GCT of the bone.

Adult↗

Penetrating keratoplasty in xeroderma pigmentosum. Case reports and review of the literature.

Xeroderma pigmentosum is an uncommon inherited disorder characterized by hypersensitivity to ultraviolet radiation, with defective repair of DNA damage caused by short-wavelength radiation. Corneal complications of this disorder may require penetrating keratoplasty for visual rehabilitation. Surgery is rarely undertaken in these eyes due to multiple associated problems involving the ocular surface and the lids. We report three cases of successful penetrating keratoplasty in xeroderma pigmentosum and review nine cases reported earlier. Successful grafts were achieved in all 12 eyes initially. Persistent superficial punctate keratopathy was observed in one eye and graft rejection episodes in five eyes. However, graft failure occurred due to an untreated rejection episode in only one eye. Another eye was treated by exenteration for recurrent ocular malignancies. This report highlights the encouraging results of penetrating keratoplasty in carefully selected patients of xeroderma pigmentosum with corneal pathology.

Adult↗

Cavernous hemangioma of the orbit: a case report.

Cavernous hemangioma is the most common benign intraorbital tumor in the young and middle aged, producing painless proptosis. It is common in females in whom it may enlarge during pregnancy. There have however been very few series reported on this entity.

Adult↗