Dr Rajesh Jhorawat, MD, DM(Nephrology) - SMS Medical College and Hospital, Jaipur - DM Nephrology

Dr Rajesh Jhorawat

MD, DM(Nephrology)

SMS Medical College and Hospital, Jaipur

DM Nephrology

Jaipur, Rajasthan | India

Main Specialties: Nephrology

Additional Specialties: Nephrology

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Dr Rajesh Jhorawat, MD, DM(Nephrology) - SMS Medical College and Hospital, Jaipur - DM Nephrology

Dr Rajesh Jhorawat

MD, DM(Nephrology)


Dr. Rajesh Jhorawat did his MBBS from prestigious All India Institute of Medical Sciences (AIIMS) New Delhi, MD from PGI Chandigarh & DM (Nephrology) from SMS Medical College Jaipur.
Dr Jhorawat has Experience in Clinical Immunology (including Transplant Immunology) from SGPGI (Lucknow) & published many papers in index journal. His study & his work have been selected for presentation both in national & international Nephrology Meet.
He is active member of-
Indian Society of Nephrology (ISN)
American Society of Nephrology (ASN)
European Renal Association (ERA - EDTA)
International Society of Nephrology (ISN)

Primary Affiliation: SMS Medical College and Hospital, Jaipur - Jaipur, Rajasthan , India


Additional Specialties:

Research Interests:

View Dr Rajesh Jhorawat’s Resume / CV


Aug 2012
SMS Medical College Jaipur
DM (Nephrology)
Dec 2009
PGIMER Chandigarh
MD (Medicine)
From Jan 2006 to Dec 2009
Dec 2005
AIIMS New Delhi
From Aug 2000 to Dec 2005


Aug 2011
SGPGI Lucknow
Worked for 7 months in Clinical Immunology Department with full exposure to Rheumatology and immunologic tests
Jan 2010
PGIMER Chandigarh
worked for one and half year in Internal medicine department with full exposure to hematology, rheumatology, emergency medicine and geriatric medicine
Jan 2006
AIIMS PSM dedartment
worked in Community Medicine at community level




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4PubMed Central Citations

Comparison of intradermal route and dose of Hepatitis B vaccine administration in chronic dialysis patients: A pilot study.

Saudi J Kidney Dis Transpl 2018 Mar-Apr;29(2):376-380

Department of Nephrology, SMS Medical College and Hospital, Jaipur, Rajasthan, India.

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http://dx.doi.org/10.4103/1319-2442.229283DOI Listing
April 2018
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Factors affecting insulin resistance and its relation to Vitamin D status and clinical nutritional parameters in dialysis patients: A single-center Indian study

Indian journal of nephrology 28 (1), 41

Indian journal of nephrology 28 (1), 41

Factors Affecting Insulin Resistance and Its Relation to Vitamin D Status and Clinical Nutritional Parameters in Dialysis Patients: A Single-center Indian Study

Address for correspondence: Dr. R. Jhorawat, SMS Medical College and Hospital, Jaipur - 302 004, Rajasthan, India. E-mail: moc.liamg@0002tawarohj
This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.


Despite new advances in the treatment of chronic kidney disease (CKD), it remains an important public health challenge.[1] CKD is a major risk factor for cardiovascular disease, which is the leading cause of mortality in these patients. Cardiac mortality in dialysis patients is more than 10-fold greater than that of the general population.[2] The excess cardiovascular mortality in patients with CKD is not fully explained by traditional risk factors such as hypertension, hypercholesterolemia, and smoking. One of the factors which were neglected in earlier studies was insulin resistance (IR) in CKD. IR which is a central pathogenic mechanism in metabolic syndrome and recognized in CKD patients has been directly associated with increased cardiovascular mortality in many studies.[3,4]

IR can be physiologic (e.g., in pregnancy) or pathologic as in CKD and it is linked to protein energy wasting and malnutrition in dialysis patients.[5,6] Hyperinsulinemic-euglycemic clamp is the gold standard for IR determination because it provides a direct measure of whole-body sensitivity to insulin. Other is oral glucose tolerance test primarily measuring glucose tolerance, which reflects both IR and beta-cell function. However, due to the complexity of these methodologies, more practical methods such as homeostatic model assessment (HOMA) and the quantitative insulin sensitivity check index are widely used in clinical studies.[7]

The role of Vitamin D deficiency in several pathological conditions has been the focus of several investigations in the last few years.[8] The complexity of the biological role of Vitamin D metabolism makes it difficult to clearly delineate the role of Vitamin D cascade in this complex pathophysiology of IR. In CKD, Vitamin D status has been related to IR; however, very limited information is available on dialysis patients and factors affecting IR. We designed this study to assess the IR in dialysis patients and its relation with Vitamin D status.

Materials and Methods

Study design

It was a cross-sectional, observational study.

Study population

We included 55 patients both on maintenance hemodialysis and peritoneal dialysis (HD and PD). The inclusion criteria were those who were on regular maintenance dialysis either on PD or HD and had age more than 18 years. Both diabetic and nondiabetic patients were included. The exclusion criteria were as follows:

  • Age <18 years
  • On insulin therapy
  • On active Vitamin D therapy
  • Chronic cardiac, hepatic, pulmonary, or thyroid disease
  • Malignancies
  • HBV-, HCV-, and HIV-positive patients
  • Patients who did not give informed consent.

This study was approved by our local ethics committee and written consent was obtained from all included patients.

Biochemical analysis

We measured blood hemoglobin level, serum creatinine, serum urea, serum calcium, serum phosphorus, serum alkaline phosphatase (ALP), serum albumin, and serum uric acid before starting HD and in the morning before starting PD. The morning fasting blood sugar and blood insulin level were measured. The homoeostasis model (HOMA) was used for the assessment of IR with the following formula:[9]

HOMA-IR (mmol/l × mU/ml) = fasting plasma glucose (mmol/l) × Fasting plasma insulin (mU/ml)/22.5.

25-(OH) Vitamin D level was measured using CLIA system, with Immulite 2000, Advia Centaur XP-Siemens system.

Nutritional assessments

Parameters such as weight (kg), heights (m), body mass index (BMI), mid-arm circumference (MAC), mid-arm muscle circumference (MAMC), total body fat, lean body weight (LBW), and subjective global assessment (SGA) were measured of all included patients [Supplement][10,11,12].


Statistical analysis

The statistical analyses were carried out using Statistical Package for Social Sciences for Windows version 20 (SPSS Chicago, IL, USA). The univariate analyses were expressed as mean ± standard deviation or percentages. ANOVA was used for comparison of the groups of SGA and their HOMA-IR index. HOMA-IR of two groups was compared using Mann–Whitney test, i.e., male versus females and HD versus PD and the correlation between nonparametric data was estimated using Spearman's coefficient. P < 0.05 was considered statistically significant.


Characteristics of dialysis patients

A total of 55 diabetic and nondiabetic patients on dialysis were included in our study. Their demographic and laboratory profile are shown in Table 1. Forty-one (74.55%) patients were male. The mean age was 37.44 ± 14.96 years, height was 166.24 ± 8.66 cm, body weight was 52.81 ± 10.21 kg, LBW was 44.81 ± 7.81 kg, body fat percentage was 14.6 ± 8.80, body fat weight was 8 ± 6.15 kg, fat weight–to-LBW ratio was 0.18 ± 0.14, LBW index was 16.13 ± 2, and BMI was 19.06 ± 3.16. The cause of end-stage renal disease was chronic glomerulonephritis in 15 patients (27.27%), hypertension in seven patients (12.73%), diabetic nephropathy in seven patients (12.73%), polycystic kidney disease in two patients (3.64%), and unknown in 24 (43.64%). The estimated glomerular filtration rate by Cockcroft–Gault formula was 7.82 ± 3.04 ml/min/1.73 m2.

As per SGA, all patients have some degree of malnutrition. Six patients had mild degree of malnutrition (10.9%), 46 patients had moderate degree of malnutrition (83.64%), and three patients had severe degree of malnutrition (5.46%). As per BMI, thirty patients were <19 kg/m2 (54.55%), 23 patients were between 19 and 25 kg/m2 (41.82%), and two were >25 kg/m2 (3.64%). Of 55 patients, 42 were on HD (73.36%) and 13 patients were on PD (23.64%).

Relationship of insulin resistance with Vitamin D and other measured parameters

Age, hemoglobin level, serum albumin, and serum uric acid had positive correlation with IR; however, only uric acid level had significant association (r = 0.303, 95% confidence interval [CI] 0.021–0.534, P = 0.025) [Table 2]. Duration of dialysis, serum ALP, parathyroid hormone, and Vitamin D level had negative correlation; however, only Vitamin D level < 20 ngm/ml had significantly higher IR (3.743 ± 4.367) compared to those with Vitamin D level >20 ngm/ml (1.673 ± 1.473 (P = 0.018) as shown in Figure 1a.

Relationship between insulin resistance and nutrition parameters

Of all the measured nutritional parameters as detailed in Table 3, lean BMI (r = 0.375, 95% CI: 0.099–0.669, P = 0.005), MAC (r = 0.377, 95% CI: 0.115–0.586, P = 0.004), MAMC (r = 0.380 95% CI: 0.121–0.579, P = 0.004), and BMI (r = 0.451, 95% CI: 0.231–0.717, P = 0.001) had significant positive association with IR. Body fat percentage did not had strong correlation in our study; however, body fat weight had achieved significant association with IR (r = 0.275, 95% CI: 0.038–0.531, P = 0.041).

The mean HOMA-IR index in mild, moderate, and severe grade malnutrition by SGA was 2.54 ± 1.55, 3.27 ± 4.17, and 2.39 ± 2.05, respectively (P = 0.861). The IR between male and female was 3.12 ± 3.69 and 2.44 ± 2.55, respectively (P = 0.528). HOMA-IR index in HD and PD patients was 3.101 ± 4.223 (P = 0.277) [Figure 1b]. Diabetic patients who were on dialysis had IR similar with that of nondiabetic patients on dialysis in our study (2.774 ± 1.800 vs. 3.194 ± 4.087, P = 0.647).


We studied dialysis patients and majority were male; however, the IR was not different in either gender in our study group (P = 0.528). The mean Vitamin D level was 15.91 ± 7.98 ng/ml and majority were Vitamin D deficient. In our study, the prevalence values of Vitamin D deficiency <10 ng/ml, <20 ng/ml, and <30 ng/ml levels were 23.64%, 70.91%, and 96.36%, respectively. Studies have reported 70%–80% prevalence of Vitamin D deficiency in CKD patients which worsens with deteriorating renal function.[13,14] The mode of dialysis did not affect IR in dialysis patients in our study (P = 0.277). In an earlier study, both HD and PD had shown similar improvement in IR after initiation of dialysis.[15]

The Vitamin D and IR had nonsignificant negative correlation; however, in subgroup analysis, patients with Vitamin D level <20 ng/ml had significantly high IR compared to those with Vitamin D level >20 ng/ml [Figure 1a]. There is also experimental evidence that Vitamin D is related to IR, a condition frequently observed in patients with progressive renal disease.[16] Earlier study by Chonchol and Scragg also support our finding and had shown that renal dysfunction and Vitamin D have independent inverse associations with IR.[17]

Another important association of IR is with serum uric acid level which has been considered as a potential risk factor in the development and progression of CKD.[18] IR has significant positive correlation with serum uric acid (r = 0.303 95% CI: 0.021–0.534, P = 0.025). This is not new in metabolic syndrome patients. However, in our study, this association reflects significance of uric acid in dialysis patients also.

One of the most important predictive factors for survival on dialysis is the presence of malnutrition.[19,20] Moreover, most of the patients in our study were malnourished. The mean BMI was 19.055 ± 3.161 kg/m2 and more than 50% patientshave BMI <19 kg/m2. As measured by SGA, around 80% patients had moderate grade malnutrition. Out of the measured parameters, BMI, MAC, MAMC, and body fat content had significant positive correlation with IR [Figure 2 and Table 2]. This means that muscle mass and body fat have significant associations with IR in dialysis patients. Other studies also have reported significant positive correlation of BMI and body fat with IR.[21,22]

Although the exact mechanism for IR in CKD remains unclear, a postreceptor defect in the insulin-receptor signaling pathway in skeletal muscle is the likely primary abnormality.[23] Siew et al. have highlighted that IR is an important determinant of protein breakdown in CKD.[24] It appears that in CKD patients requiring dialysis, skeletal muscle is the primary tissue which is responsible for IR. In our study, IR increases with skeletal muscle mass; however, in sarcopenic patients, other factors such as metabolic acidosis, inflammation, and oxidative stress might be the main contributors of IR.

There are many limiting factors in our study. First, inflammatory state of the patient which is an important mechanism of IR in CKD has not mean measured and needs a well-controlled study. Second, visceral fat which has been reported in some studies to be related with IR has not been measured in our study. Third, dual-energy X-ray absorptiometry or bioimpedance was not used in our study. Finally, IR was quantified using the surrogate index of HOMA, and these findings need to be confirmed using euglycemic clamp technique.


Serum uric acid and Vitamin D level <20 ng/ml significantly influence the insulin sensitivity in dialysis patients. Anthropometric measures which indicate body muscle mass are more strongly correlated with IR in dialysis patients. It appears that the milieu in CKD is different, where IR is less likely depended on underlying causes and mode of dialysis. However, IR is a potentially modifiable cardiovascular risk factor and more studies are required in the future regarding intervention for preventing IR and its effect on cardiovascular morbidity.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


1. Kasiske BL, Chavers B, Foley R. K/DOQI clinical practice guidelines for chronic kidney disease: Evaluation, classification, and stratification. Am J Kidney Dis. 2002;39(Suppl 1):1–299.
2. Foley RN, Parfrey PS, Sarnak MJ. Clinical epidemiology of cardiovascular disease in chronic renal disease. Am J Kidney Dis. 1998;32(5 Suppl 3):S112–9. [PubMed: 9820470]
3. Chen J, Gu D, Chen CS, Wu X, Hamm LL, Muntner P, et al. Association between the metabolic syndrome and chronic kidney disease in Chinese adults. Nephrol Dial Transplant. 2007;22:1100–6. [PubMed: 17272313]
4. Thomas G, Sehgal AR, Kashyap SR, Srinivas TR, Kirwan JP, Navaneethan SD. Metabolic syndrome and kidney disease: A systematic review and meta-analysis. Clin J Am Soc Nephrol. 2011;6:2364–73. [PMCID: PMC3186450] [PubMed: 21852664]
5. Semple D, Smith K, Bhandari S, Seymour AM. Uremic cardiomyopathy and insulin resistance: A critical role for Akt? J Am Soc Nephrol. 2011;22:207–15.[PubMed: 20634295]
6. Shinohara K, Shoji T, Emoto M, Tahara H, Koyama H, Ishimura E, et al. Insulin resistance as an independent predictor of cardiovascular mortality in patients with end-stage renal disease. J Am Soc Nephrol. 2002;13:1894–900. [PubMed: 12089386]
7. Shoji T, Emoto M, Nishizawa Y. HOMA index to assess insulin resistance in renal failure patients. Nephron. 2001;89:348–9. [PubMed: 11598402]
8. Lips P. Vitamin D physiology. Prog Biophys Mol Biol. 2006;92:4–8. [PubMed: 16563471]
9. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: Insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia. 1985;28:412–9. [PubMed: 3899825]
10. Durnin JV, Womersley J. Body fat assessed from total body density and its estimation from skinfold thickness: Measurements on 481 men and women aged from 16 to 72 years. Br J Nutr. 1974;32:77–97. [PubMed: 4843734]
11. Siri W. Body composition from fluid spaces and density: Analysis of methods. In: Brozek J, Hanschel A, editors. Techniques for Measuring Body Composition.Washington, DC: National Academy of Sciences; 1961. pp. 223–44.
12. Steiber AL, Kalantar-Zadeh K, Secker D, McCarthy M, Sehgal A, McCann L. Subjective Global Assessment in chronic kidney disease: A review. J Ren Nutr. 2004;14:191–200. [PubMed: 15483778]
13. LaClair RE, Hellman RN, Karp SL, Kraus M, Ofner S, Li Q, et al. Prevalence of calcidiol deficiency in CKD: A cross-sectional study across latitudes in the United States. Am J Kidney Dis. 2005;45:1026–33. [PubMed: 15957131]
14. Bhan I, Burnett-Bowie SA, Ye J, Tonelli M, Thadhani R. Clinical measures identify Vitamin D deficiency in dialysis. Clin J Am Soc Nephrol. 2010;5:460–7.[PMCID: PMC2827576] [PubMed: 20185603]
15. Kobayashi S, Maejima S, Ikeda T, Nagase M. Impact of dialysis therapy on insulin resistance in end-stage renal disease: Comparison of haemodialysis and continuous ambulatory peritoneal dialysis. Nephrol Dial Transplant. 2000;15:65–70. [PubMed: 10607769]
16. Zittermann A. Vitamin D and disease prevention with special reference to cardiovascular disease. Prog Biophys Mol Biol. 2006;92:39–48. [PubMed: 16600341]
17. Chonchol M, Scragg R. 25-Hydroxyvitamin D, insulin resistance, and kidney function in the Third National Health and Nutrition Examination Survey. Kidney Int. 2007;71:134–9. [PubMed: 17082756]
18. Kanbay M, Yilmaz MI, Sonmez A, Solak Y, Saglam M, Cakir E, et al. Serum uric acid independently predicts cardiovascular events in advanced nephropathy. Am J Nephrol. 2012;36:324–31. [PubMed: 23007099]
19. Acchiardo SR, Moore LW, Latour PA. Malnutrition as the main factor in morbidity and mortality of hemodialysis patients. Kidney Int Suppl. 1983;16:S199–203.[PubMed: 6429404]
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23. Siew ED, Ikizler TA. Insulin resistance and protein energy metabolism in patients with advanced chronic kidney disease. Semin Dial. 2010;23:378–82. [PubMed: 20701717]
24. Siew ED, Pupim LB, Majchrzak KM, Shintani A, Flakoll PJ, Ikizler TA. Insulin resistance is associated with skeletal muscle protein breakdown in non-diabetic chronic hemodialysis patients. Kidney Int. 2007;71:146–52. [PubMed: 17063174]

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January 2018
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Preventive role of carvedilol in adriamycin-induced cardiomyopathy

Indian J Med Res 2016 Nov;144:725-729

Indian J Med Res

Background & objectives: Adriamycin though considered as an effective anticancer drug, leads to irreversible cardiomyopathy (CMP) and congestive heart failure (CHF). The aim of this study was to determine the protective effect of carvedilol in adriamycin (ADR)-induced cardiomyopathy (CMP) in cancer patients. Methods: Patients with lymphoreticular malignancy in whom ADR therapy was planned were randomized into two groups: carvedilol and control. Twenty seven patients each were enrolled in carvedilol and control groups. In the carvedilol group, 12.5 mg once daily oral carvedilol was given during six months. The patients were evaluated by echocardiography before and after chemotherapy. Left ventricular ejection fraction (EF) and systolic and diastolic diameters were calculated. Results: At six months of follow up, six patients in the carvedilol group and five in the control group had died. The mean EF (63.19 vs. 63.88%) and fraction shortening (FS) (34 vs. 34.6) of the carvedilol group were similar at follow up, but in the control group, the mean EF (67.27 vs. 60.82%, P=0.003) and FS (38.48 vs. 34.6, P<0.05) at control echocardiography were significantly lower. In carvedilol group, both systolic and diastolic diameters were not changed, but in control group, systolic diameters were significantly increased compared with basal measures (left ventricular end systolic diameter = 28.26±5.50 mm vs. 31.25± 6.50 mm; P< 0.05). Interpretation & conclusions: Prophylactic use of carvedilol in patients receiving anthracycline protected systolic functions of the left ventricle. Carvedilol can be a potential drug which can ameliorate ADRinduced CMP.

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November 2016
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Acute kidney injury in patients with Plasmodium vivax malaria: Clinicohistopathological profile

Saudi Journal for Health Sciences. 2016 Sep-Dec;5(3):138-41

Saudi Journal for Health Sciences

Context: There has been an unexplained increase in the number of cases with multiorgan dysfunction including acute kidney injury (AKI), attributed to Plasmodium vivax monoinfection. Only a few case reports in literature have published the renal biopsy findings in these patients. Aims: The aim of this study was to evaluate the clinical and histopathologic profile of patients with P. vivax malaria monoinfection and AKI. Settings and Design: A prospective study was performed in a tertiary care hospital in North‑Western India. Subjects and Methods: The study included patients diagnosed with P. vivax monoinfection on peripheral smear blood films and rapid diagnostic test (positive for P. vivax specific lactate dehydrogenase). AKI was defined based on the WHO criteria for complicated malaria, i.e. serum creatinine >265 μmol/l or 3 mg/dl. The patients were initiated on hemodialysis for persistent hyperkalemia, fluid overload, severe metabolic acidosis, or uremic symptoms. Renal biopsy was performed in the presence of active urinary sediments (proteinuria, hematuria) or persistence of renal failure >14 days. Results: A total of thirty patients fulfilled AKI criteria. The patients with AKI were older (mean age 42.1 ± 10.9 years), male, with a longer duration of illness (mean 12.3 ± 10 days) and associated with multisystem dysfunction. The mean serum creatinine was 7.58 ± 3.2 mg/dl, thrombocytopenia was seen in 47%. Thirty percent had severe anemia requiring a blood transfusion. Renal biopsy was performed in six patients for various indications. The most common pattern was acute tubular necrosis (four patients), followed by acute cortical necrosis (1), and thrombotic microangiopathy (one patient). The complete renal recovery was seen in 24 (80%). Two patients became dialysis‑dependent. Conclusions: AKI associated with P. vivax monoinfection is not rare as previously thought. Therefore, it should be considered in the differential diagnosis of any patient presenting with AKI.

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September 2016
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Effect of vitamin D level on the immunogenicity to hepatitis B vaccination in dialysis patients.

Indian J Gastroenterol 2016 Jan 15;35(1):67-71. Epub 2016 Feb 15.

Department of Nephrology, Sawai Man Singh Medical College and Hospital, J L N Marg, Jaipur, 302 004, India.

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January 2016
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Can Analgesic-abuse Nephropathy is a Fertile Groundfor for Rare Collecting Duct (Bellini Duct) Renal Cell Carcinoma or Merely a Coincidence?

Indian journal of pharmaceutical sciences 78 (1), 159

Indian journal of pharmaceutical sciences

Can Analgesic-abuse Nephropathy is a Fertile Groundfor for Rare Collecting Duct (Bellini Duct) Renal Cell Carcinoma or Merely a Coincidence?

Address for correspondence: E-mail: moc.liamg@0002tawarohj
Received 2014 Dec 4; Revised 2015 Nov 13; Accepted 2016 Feb 8.
This is an open access article distributed under the terms of the Creative Commons Attribution NonCommercial ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non commercially, as long as the author is credited and the new creations are licensed under the identical terms.

Non-steroidal antiinflammatory drugs (NSAIDs) are one of the most commonly prescribed drugs, especially in chronic inflammatory disease. However, they are not without side effect that including acute and chronic, can range from reversible ischemia to chronic kidney disease and urothelial tumors to renal cell carcinoma (RCC). The NSAIDs has been implicated in the causation of the papillary subtype of RCC[1].

Collecting duct (Bellini duct) renal cell carcinoma (CDRCC) occurring in 0.4-2.0% of cases of renal cell carcinoma (RCC) which make us to depend on case report or case series for our knowledge to this rare subtype. Till now we have indirect evidence of relationship of NSAIDs in the causation of CDRCC. This is perhaps the first case, in which NSAIDs are directly related in the causation of this rare subtype.

This was a case of thirty eight years old young male who was symptomatic for last twenty two years with low back pain and bilateral pain and swelling in ankle joints with early morning stiffness. No pain and swelling in other joints. He consulted a physician and was started on pain killer containing diclofenac and paracetamol (acetaminophen) combination, which relieved his pain significantly. Thereafter, he used to take the same medication whenever he feels increase or worsening of his back pain. He was not on regular follow up to any physician and continue to consume this medication for >15 years.

Now, after twenty years, he was admitted with symptoms of generalized body swelling and headache. He was found to be hypertensive and excreting proteins in his urine in nephrotic range (24 h urine protein=4944 g total volume=1600 ml). The abdomen sonography was showing mass in his right kidney (lower pole) and contracted 'ral kidney´. His renal function test was deranged (serum creatinine=5.7 mg/dl, serum urea=157 mg/dl and was anemic (hemoglobin=7.8 gm/dl). Other investigation was [Na+]=140 mEq/l, [K+]=5.3 mEq/l, serum albumin=3.0 g/dl, serum total protein=5.8 g/dl, serum alkaline phosphate=89 IU/l, serum cholesterol=231 mg/dl. He was evaluated for his basic disease. X-ray pelvis was showing bilateral fused sacroiliac joints (fig. 1a). MRI abdomen confirmed solid mass in the right kidney (fig. 1b). HLA-B27 was positive and rheumatoid factor was negative with raise ESR and positive CRP (qualitative). The diagnosis of ankylosing spondylitis with analgesic-abuse nephropathy (secondary FSGS) and incidental detected renal mass? RCC was made. The right side nephrectomy was done with histopathology of the mass was showing collecting duct type RCC (CDRCC), as shown in fig. 1c and fig. 1d. He remains dialysis dependent during follow up. He was on regular hemodialysis for one and a half month; however, he demised after 2 months.

As we know NSAIDs are drugs with 'two-edge sword'. Use of certain analgesics, including aspirin and non-aspirin NSAIDs have been associated with reduced risk of breast, prostate, and colorectal cancers. On the other hand, they increase the risk of urinary tract carcinoma and RCC. Recently, a comprehensive meta-analysis of studies dedicated to the relationship between the three most commonly used analgesics (acetaminophen, aspirin and non-aspirin NSAID) and kidney cancer risk, had shown that acetaminophen and non-aspirin NSAIDs increased the risk of RCC[1]. In our case also, he was consuming paracetamol (acetaminophen) and diclofenac for more than a decade which might predispose him for RCC.

NSAIDs are reported to increase both RCC and uroepithelial tumors. Rocha et al. in their study on rat had shown that aspirin, salicylic acid and acetaminophen reduced number of rapidly proliferating cell by 50% in inner medullary collecting duct[2]. Acetaminophen, in addition, arrests most cell in late G1 and S phase[3]. It produced mixed form of cell death with both oncosis (swollen cells and nuclei) and apoptosis. Acetaminophen inhibits DNA synthesis and cause chromosomal aberration due to inhibition of ribonucleotide reductase. These genotoxic effects have been postulated in carcinogenesis due to NSAIDs[2].

CDRCC are distinct tumors from clear cell RCC (CCRCC) which is a most common renal tumor. CDRCC develops from the collecting ducts in the renal medullary pyramid, whereas CCRCC arise from the convoluted tubules. There are no specific CT findings to distinguish CDRCC from CCRCC although medullary location, weak and heterogeneous enhancement, renal sinus involvement, infiltrative growth with preserved renal contours and a cystic component are frequently seen. Tumor cell in CDRCC show positivity with antibodies to Ulex European agglutinin 1 lectin, peanut agglutinin (PNA), vimentin, lysozyme, distal tubular markers (e.g EMA and high molecular weight cytokeratin) and negative for proximal tubular markers[4]. These markers, however, are not tested in our case.

In the available literature, CDRCC is indirectly related to NSAIDs. There is a case report, which highlighted co-existence of two subtype of RCC in the same individual at the same time i.e CDRCC and papillary RCC[4]. Another case report, which mention the occurrence of CDRCC subtype simultaneously with transitional cell carcinoma (TCC) in a same individual at the same time[5]. Both these tumors which were co-existent with CDRCC had been reported with NSAIDs as their risk factor. In addition, CDRCC shares some histological similarities and site of origin with papillary subtype of RCC and some common genetic abnormalities with TCC. Ours is the first case in which NSAID exposure directly reported to be associated with CDRCC. As CDCC has a very low incidence of all renal tumors, as a result, our knowledge of this tumor is limited.

In conclusion, CDRCC is a rare and aggressive subtype of RCC. Our available knowledge for this tumor arises from small case series and case reports. And our case directly relates that long exposure of acetaminophen and NSAIDs might be a risk factor for CDRCC also.

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Conflicts of interest:

There are no conflicts of interest.


Jhorawat, et al.: Is AAN a Risk Factor for CDRCC?


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January 2016
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Plasmodium vivax induced hemolytic uremic syndrome: An uncommon manifestation that leads to a grave complication and treated successfully with renal transplantation.

Trop Parasitol 2015 Jul-Dec;5(2):127-9

Department of Nephrology, SMS Medical College and Hospital, SMS Hospital, Jaipur, Rajasthan, India.

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http://dx.doi.org/10.4103/2229-5070.162528DOI Listing
December 2015
36 Reads

A comparative study of central versus posterior approach for internal jugular hemodialysis catheter insertion.

Indian J Nephrol 2015 Sep-Oct;25(5):265-8

Department of Nephrology, SMS Hospital and Medical College, Jaipur, Rajasthan, India.

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http://dx.doi.org/10.4103/0971-4065.151356DOI Listing
December 2015
17 Reads
1 Citation


Nephrology Dialysis Transplanation 30 (suppl_3), iii336-iii337

Nephrology Dialysis Transplanation 30 (suppl_3), iii336-iii337

Rajesh Jhorawat1, Neha Bansal1, Mohit Mathur1, Dharmindra Prasad1,
Piyush Kimmatkar
1, Pankaj Beniwal1, Dhananjay Agarwal1 and Vinay Malhotra1
1SMS Medical College and Hospital, Nephrology, Jaipur, India
Introduction and Aims: To measure Insulin resistance in dialysis patients and its
relation to vitamin D status and nutritional parameters
Methods: We included 55 patients on maintenance dialysis. Insulin resistance was
measured by HOMA-IR index defined as fasting serum Insulin (µU/L) X Fasting blood
sugar (mmol/L) /22.5. Baseline vitamin D levels were measured by chemiluminescence
immunoassay (CLIA) method. HOMA-IR index correlated with nutrition parameters
like seven points Subjective Global assessment (SGA) and anthropometric measures,
e.g. body fat percentage, lean body mass (LBM), Lean body mass index (LBMI), body
mass index (BMI), mid arm circumference (MAC) and mid arm muscle circumference
Results: Total 55 patients studied with 74.55% are males. The prevalence of vitamin D
deficiency <10 ngm/ml, <20 ngm/ml and <30 ngm/ml levels are 96.36%, 70.91% and
23.64% respectively. Mean HOMA-IR index is 3.14 ± 3.86. The measured parameter
which has a significant positive correlation with insulin resistance is serum uric acid
(r= 0.303, r2=0.092, 95 %CI= 0.021 to 0.534 and p=0.025). In nutritional assessment,
parameters like BMI, MAC and MAMC have statistically significant positive correlation
with HOMA-IR index (p=<0.001, 0.004 and 0.004 respectively). SGA does not have a
significant association with insulin resistance. The correlation of HOMA-IR with
vitamin D is negative (r= - 0.140 r2=0.02, 95 %CI= -0.397 to 0.138 and p=0.309),
however, in subgroup analysis patient with vitamin D level < 20ngm/ml have
significantly high Insulin resistance compare to those with vitamin D >20ngm/ml i.e
3.743±4.367 and 1.673±1.473 respectively (p=0.018). Mode of dialysis did not have a
significant effect on insulin resistance (HD vs PD, p=0.227)
Conclusions: Majority patients on maintenance dialysis are vitamin D deficient.
Vitamin D level, especially <20 ngm/ml is likely to have more insulin resistance
compare to higher level. Insulin resistance in dialysis patients has significant positive
association with BMI, MAC and MAMC along with serum uric acid.

resenting as bilateral cortical
blindness. Indian J Med Sci 2017;69:59
Source of support:
Conflict of Interest:
None declared

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May 2015

Renal cortical necrosis: A rare complication of Plasmodium vivax malaria.

Indian J Nephrol 2014 Nov;24(6):390-3

Professor and Head, Department of Nephrology, SMS Medical College, Jaipur, Rajasthan, India.

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http://dx.doi.org/10.4103/0971-4065.133789DOI Listing
November 2014
43 Reads
2 Citations

Effect of renal transplantation on multiple hormone levels in patients of chronic kidney disease: A single center study

Indian journal of transplantation 2014 July-September 8(3);75-79

Indian journal of transplantation

Aim To assess the level of hormones in chronic kidney disease (CKD) patients and the effect of renal transplantation (RTx) on these hormones. Materials and methods 17 patients enrolled and levels of 11 hormones i.e. FT3, FT4, TSH, FSH, LH, prolactin, testosterone, cortisol, growth hormone, PTH and insulin were measured in every patient before and at 1st, 3rd and 6th month after RTx with correlation to serum creatinine. Patients with underlying endocrine disorders were excluded. Result At 1st and 3rd month of follow up after RTx, there was no statistical significant change in the hormones level except in PTH, which normalised (Pre transplant levels: 262.542 ± 239.706 and 1 month levels: 101.412 ± 66.615 p = 0.024 at 3rd month level: 113.02 ± 95.960 p = 0.036). At 6th month, along with PTH, LH level decreased significantly (LH level pre-RTx 8.387 ± 4.536 and 3.091 ± 2.139 at 6th month p = 0.024). Levels of other hormones also normalised. Mean serum creatinine at 6th month had increased from its nadir level post RTx (1.149 ± 0.164 mg/dl to 1.386 ± 0.323 mg/dl p = 0.034), due to rise of serum creatinine in 4 patients. FT3, cortisol, prolactin and insulin levels also increased in parallel with serum creatinine, however insulin level correlated significantly (r = 0.759 with 95% CI = 0.015–0.962). Conclusion RTx corrects most of the hormonal disturbances in CKD patients, particularly abnormalities in PTH and LH levels in early post transplant period. Even mild allograft dysfunction significantly affects the hormonal levels in a manner which is similar to the changes seen in CKD.

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August 2014
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