Letters to Editor
We showed that NLR, which is an important indicator of inflammation, was significantly increased in patients with community‑acquired acute renal failure. Elevated NLR is a predictor of long‑term mortality and bad prognosis; it can also be used in acute inflammatory conditions. The immune system of patients treated in the intensive care unit rapidly responds to systemic inflammation or sepsis. Neutrophilia and lymphocytopenia are related to disease severity. As the clinical condition worsens, neutrophilia and lymphocytopenia become significant and NLR is increased. NLR can be used as a parameter of disease severity in patients treated at the intensive care unit.[2] In our study, NLR was high at the time of acute renal failure diagnosis and decreased when renal function recovered. The mean duration of acute renal failure recovery was 7.8 days. As neutrophils and lymphocytes give more rapid response to the severity of inflammation, NLR can be used for monitoring acute inflammatory conditions. Studies are needed to evaluate the prognostic/diagnostic utility of NLR in monitoring acute inflammatory conditions and acute renal failure. E. Erdem Department of Nephrology, Trabzon Kanuni Education and Research Hospital, Trabzon, Turkey Address for correspondence: Dr. Emre Erdem, Department of Nephrology, Trabzon Kanuni Education and Research Hospital, Trabzon, Turkey. E-mail: [email protected]
References 1.
Akcay A, Nguyen Q, Edelstein CL. Mediators of inflammation in acute kidney injury. Mediators Inflamm 2009;2009:137072. 2. Zahorec R. Ratio of neutrophil to lymphocyte counts‑‑Rapid and simple parameter of systemic inflammation and stress in critically ill. Bratisl Lek Listy 2001;102:5‑14. 3. Erdem E, Kaya C, Karataş A, Dilek M, Akpolat T. Neutrophil to lymphocyte ratio in predicting short‑term mortality in hemodialysis patients. J Exp Clin Med 2013; 30:129‑32. 4. An X, Mao HP, Wei X, Chen JH, Yang X, Li ZB, et al. Elevated neutrophil to lymphocyte ratio predicts overall and cardiovascular mortality in maintenance peritoneal dialysis patients. Int Urol Nephrol 2012;44:1521‑8. 5. Azab B, Jaglall N, Atallah JP, Lamet A, Raja‑Surya V, Farah B, et al. Neutrophil‑lymphocyte ratio as a predictor of adverse outcomes of acute pancreatitis. Pancreatology 2011;11:445‑52. Access this article online Quick Response Code:
Website: www.indianjnephrol.org DOI: 10.4103/0971-4065.145099
Membranous nephropathy associated with the use of levodopa‑carbidopa combination Sir, Membranous nephropathy (MN) is the cause of nephrotic syndrome in approximately 25% of adults.[1] In over 75% of patients of MN, no aetiological agent can be determined. Drugs account for 6–9% of secondary MN.[2] Drug associated MN can develop at any age and typically develops soon after exposure to the offending agent.[3] The classic offenders are gold, penicillamine, nonsteroidal anti‑inflammatory drugs and captopril, though there are reports for many other drugs. We could not find, after a thorough literary search a single report of levodopa‑carbidopa combination associated with MN. We present a 45‑year‑old male patient who has been on regular follow up for Parkinson’s disease (PD) for the past 6 months. He was being treated with levodopa‑carbidopa combination, 110 mg twice a day. He presented with history of gradually worsening swelling of feet and face of 2 months duration. There was a history of oliguria and increased frothiness of urine. His blood pressure at presentation was 120/80 mmHg. Investigations were given in the Table 1. Renal biopsy showed 11 glomeruli. All glomeruli were normal in size. The capillary loops were stiff, round and patent with thick basement membrane. Silver methanamine stain showed spikes. Tubules and vascular system were unremarkable. Immunofluorescence showed diffuse Table 1: Investigations Test Hemoglobin Urine‑albumin RBC and WBC 24 h urine protein Random blood glucose Serum creatinine Total serum proteins Serum albumin Serum cholesterol Serum triglycerides HbsAg Anti HCV Ab HIV Chest radiograph Ultrasound abdomen
Result 14.7 g/dl 4+ Nil 3600 mg 103 mg/dl 0.82 mg/dl 6.0 g/dl 3.0 g/dl 224 mg/dl 365 mg/dl Negative Negative Nonreactive Normal study Kidneys: right: 9.9 cm×3.8 cm, left: 9.6 cm×3.4 cm
RBC: Red blood cell, WBC: White blood cell, HbsAg: Hepatitis B surface antigen, HCV: Hepatitis C virus, HIV: Human immunodeficiency virus
Indian Journal of Nephrology
Mar 2015 / Vol 25 / Issue 2
127
Letters to Editor
granular deposits with immunoglobulin G (IgG) 3+, IgA trace, IgM trace and C3 2+ along the capillary loops. The features were suggestive of MN. Serum anti‑phospholipase‑A (2)‑receptor (PLA2R) antibodies, done by enzyme‑linked immunosorbent assay, were negative. Suspecting that the levodopa‑carbidopa combination would be a cause of MN, it was stopped. Ropinirole 0.5 mg, half tablet bid was started. During next 4 weeks, the swelling of feet and face have disappeared, the proteinuria declined to 414 mg/day, serum total proteins and serum albumin improved to 6.7 g/ dl and 3.9 g/dl respectively. Serum anti phospholipase‑A2‑receptor antibodies are present in 70% of patients with idiopathic MN with active disease.[4] The anti‑PLA2R antibodies were found to be present in reports of patients with secondary MN. These patients were one out of 20 patients of systemic lupus erythematosus, one out of 16 patients of hepatitis B associated MN, three out of 10 patients of malignancy associated MN and one report of sarcoidosis associated MN. The accuracy of anti-PLA2R antibodies to identify idiopathic MN and to exclude secondary causes of MN awaits well‑designed prospective studies, which are currently underway.[5] In our patient, the temporal relation of use of the levodopa‑carbidopa with the onset of symptoms, the reduction of the proteinuria consequent to its stoppage and absence of anti PLA2R antibodies all pointed to a possible association of levodopa‑carbidopa combination with the MN. Spontaneous remission of the MN could also be another possibility.
128
Mar 2015 / Vol 25 / Issue 2
V. Chaitanya, B. Sangeetha, V. N. Madhav Rao1, R. Ram, B. Vengamma1, V. Siva Kumar Departments of Nephrology and 1Neurology, Sri Venkateshwara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India Address for correspondence: Dr. Ram Rapur, Department of Nephrology, Sri Venkateshwara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India. E-mail: [email protected]
References 1. Braden GL, Mulhern JG, O’Shea MH, Nash SV, Ucci AA Jr, Germain MJ. Changing incidence of glomerular diseases in adults. Am J Kidney Dis 2000;35:878‑83. 2. Cahen R, Francois B, Trolliet P, Gilly J, Parchoux B. Aetiology of membranous glomerulonephritis: A prospective study of 82 adult patients. Nephrol Dial Transplant 1989;4:172‑80. 3. Tönroth T, Skrifvars B. Gold nephropathy prototype of membranous glomerulonephritis. Am J Pathol 1974;75:573‑90. 4. Beck LH Jr, Bonegio RG, Lambeau G, Beck DM, Powell DW, Cummins TD, et al. M‑type phospholipase A2 receptor as target antigen in idiopathic membranous nephropathy. N Engl J Med 2009;361:11‑21. 5. Hofstra JM, Wetzels JF. Anti‑PLA2R antibodies in membranous nephropathy: Ready for routine clinical practice? Neth J Med 2012;70:109‑13.
Access this article online Quick Response Code:
Website: www.indianjnephrol.org DOI: 10.4103/0971-4065.145130
Indian Journal of Nephrology
Copyright of Indian Journal of Nephrology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
We showed that NLR, which is an important indicator of inflammation, was significantly increased in patients with community‑acquired acute renal failure. Elevated NLR is a predictor of long‑term mortality and bad prognosis; it can also be used in acute inflammatory conditions. The immune system of patients treated in the intensive care unit rapidly responds to systemic inflammation or sepsis. Neutrophilia and lymphocytopenia are related to disease severity. As the clinical condition worsens, neutrophilia and lymphocytopenia become significant and NLR is increased. NLR can be used as a parameter of disease severity in patients treated at the intensive care unit.[2] In our study, NLR was high at the time of acute renal failure diagnosis and decreased when renal function recovered. The mean duration of acute renal failure recovery was 7.8 days. As neutrophils and lymphocytes give more rapid response to the severity of inflammation, NLR can be used for monitoring acute inflammatory conditions. Studies are needed to evaluate the prognostic/diagnostic utility of NLR in monitoring acute inflammatory conditions and acute renal failure. E. Erdem Department of Nephrology, Trabzon Kanuni Education and Research Hospital, Trabzon, Turkey Address for correspondence: Dr. Emre Erdem, Department of Nephrology, Trabzon Kanuni Education and Research Hospital, Trabzon, Turkey. E-mail: [email protected]
References 1.
Akcay A, Nguyen Q, Edelstein CL. Mediators of inflammation in acute kidney injury. Mediators Inflamm 2009;2009:137072. 2. Zahorec R. Ratio of neutrophil to lymphocyte counts‑‑Rapid and simple parameter of systemic inflammation and stress in critically ill. Bratisl Lek Listy 2001;102:5‑14. 3. Erdem E, Kaya C, Karataş A, Dilek M, Akpolat T. Neutrophil to lymphocyte ratio in predicting short‑term mortality in hemodialysis patients. J Exp Clin Med 2013; 30:129‑32. 4. An X, Mao HP, Wei X, Chen JH, Yang X, Li ZB, et al. Elevated neutrophil to lymphocyte ratio predicts overall and cardiovascular mortality in maintenance peritoneal dialysis patients. Int Urol Nephrol 2012;44:1521‑8. 5. Azab B, Jaglall N, Atallah JP, Lamet A, Raja‑Surya V, Farah B, et al. Neutrophil‑lymphocyte ratio as a predictor of adverse outcomes of acute pancreatitis. Pancreatology 2011;11:445‑52. Access this article online Quick Response Code:
Website: www.indianjnephrol.org DOI: 10.4103/0971-4065.145099
Membranous nephropathy associated with the use of levodopa‑carbidopa combination Sir, Membranous nephropathy (MN) is the cause of nephrotic syndrome in approximately 25% of adults.[1] In over 75% of patients of MN, no aetiological agent can be determined. Drugs account for 6–9% of secondary MN.[2] Drug associated MN can develop at any age and typically develops soon after exposure to the offending agent.[3] The classic offenders are gold, penicillamine, nonsteroidal anti‑inflammatory drugs and captopril, though there are reports for many other drugs. We could not find, after a thorough literary search a single report of levodopa‑carbidopa combination associated with MN. We present a 45‑year‑old male patient who has been on regular follow up for Parkinson’s disease (PD) for the past 6 months. He was being treated with levodopa‑carbidopa combination, 110 mg twice a day. He presented with history of gradually worsening swelling of feet and face of 2 months duration. There was a history of oliguria and increased frothiness of urine. His blood pressure at presentation was 120/80 mmHg. Investigations were given in the Table 1. Renal biopsy showed 11 glomeruli. All glomeruli were normal in size. The capillary loops were stiff, round and patent with thick basement membrane. Silver methanamine stain showed spikes. Tubules and vascular system were unremarkable. Immunofluorescence showed diffuse Table 1: Investigations Test Hemoglobin Urine‑albumin RBC and WBC 24 h urine protein Random blood glucose Serum creatinine Total serum proteins Serum albumin Serum cholesterol Serum triglycerides HbsAg Anti HCV Ab HIV Chest radiograph Ultrasound abdomen
Result 14.7 g/dl 4+ Nil 3600 mg 103 mg/dl 0.82 mg/dl 6.0 g/dl 3.0 g/dl 224 mg/dl 365 mg/dl Negative Negative Nonreactive Normal study Kidneys: right: 9.9 cm×3.8 cm, left: 9.6 cm×3.4 cm
RBC: Red blood cell, WBC: White blood cell, HbsAg: Hepatitis B surface antigen, HCV: Hepatitis C virus, HIV: Human immunodeficiency virus
Indian Journal of Nephrology
Mar 2015 / Vol 25 / Issue 2
127
Letters to Editor
granular deposits with immunoglobulin G (IgG) 3+, IgA trace, IgM trace and C3 2+ along the capillary loops. The features were suggestive of MN. Serum anti‑phospholipase‑A (2)‑receptor (PLA2R) antibodies, done by enzyme‑linked immunosorbent assay, were negative. Suspecting that the levodopa‑carbidopa combination would be a cause of MN, it was stopped. Ropinirole 0.5 mg, half tablet bid was started. During next 4 weeks, the swelling of feet and face have disappeared, the proteinuria declined to 414 mg/day, serum total proteins and serum albumin improved to 6.7 g/ dl and 3.9 g/dl respectively. Serum anti phospholipase‑A2‑receptor antibodies are present in 70% of patients with idiopathic MN with active disease.[4] The anti‑PLA2R antibodies were found to be present in reports of patients with secondary MN. These patients were one out of 20 patients of systemic lupus erythematosus, one out of 16 patients of hepatitis B associated MN, three out of 10 patients of malignancy associated MN and one report of sarcoidosis associated MN. The accuracy of anti-PLA2R antibodies to identify idiopathic MN and to exclude secondary causes of MN awaits well‑designed prospective studies, which are currently underway.[5] In our patient, the temporal relation of use of the levodopa‑carbidopa with the onset of symptoms, the reduction of the proteinuria consequent to its stoppage and absence of anti PLA2R antibodies all pointed to a possible association of levodopa‑carbidopa combination with the MN. Spontaneous remission of the MN could also be another possibility.
128
Mar 2015 / Vol 25 / Issue 2
V. Chaitanya, B. Sangeetha, V. N. Madhav Rao1, R. Ram, B. Vengamma1, V. Siva Kumar Departments of Nephrology and 1Neurology, Sri Venkateshwara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India Address for correspondence: Dr. Ram Rapur, Department of Nephrology, Sri Venkateshwara Institute of Medical Sciences, Tirupati, Andhra Pradesh, India. E-mail: [email protected]
References 1. Braden GL, Mulhern JG, O’Shea MH, Nash SV, Ucci AA Jr, Germain MJ. Changing incidence of glomerular diseases in adults. Am J Kidney Dis 2000;35:878‑83. 2. Cahen R, Francois B, Trolliet P, Gilly J, Parchoux B. Aetiology of membranous glomerulonephritis: A prospective study of 82 adult patients. Nephrol Dial Transplant 1989;4:172‑80. 3. Tönroth T, Skrifvars B. Gold nephropathy prototype of membranous glomerulonephritis. Am J Pathol 1974;75:573‑90. 4. Beck LH Jr, Bonegio RG, Lambeau G, Beck DM, Powell DW, Cummins TD, et al. M‑type phospholipase A2 receptor as target antigen in idiopathic membranous nephropathy. N Engl J Med 2009;361:11‑21. 5. Hofstra JM, Wetzels JF. Anti‑PLA2R antibodies in membranous nephropathy: Ready for routine clinical practice? Neth J Med 2012;70:109‑13.
Access this article online Quick Response Code:
Website: www.indianjnephrol.org DOI: 10.4103/0971-4065.145130
Indian Journal of Nephrology
Copyright of Indian Journal of Nephrology is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
