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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2021  |  Volume : 32  |  Issue : 6  |  Page : 1813-1819
Clinical Remission of Immunoglobulin A Nephropathy after Bariatric Surgery in a Young Morbidly Obese Patient

1 Department of Nephrology, New Delhi, India
2 Institute of Medical Genetics, New Delhi, India
3 Department of Pathology, and Institute of Minimal Access, New Delhi, India
4 Institute of Minimal Access, Metabolic and Bariatric Surgery, Sir Ganga Ram Hospital, New Delhi, India
5 Department of Nephrology, Post Graduate Institute, Chandigarh, India

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Date of Web Publication27-Jul-2022


A 23-year-old girl with morbid obesity, diabetes mellitus, hypertension, obstructive sleep apnea, and immunoglobulin A nephropathy (IgAN) attended a bariatric clinic after multiple failed attempts at weight loss. In the past, she was diagnosed with IgAN with nephrotic syndrome and raised blood pressure at the age of 11 years. Apart from optimization of blood pressure with angiotensin receptor blocker, she required steroid to maintain her remission in initial four years which was later switched to mycophenolate mofetil (MMF). She was diagnosed with diabetes at the age of 13 years; her blood sugars remained poorly controlled despite therapy with oral hypoglycemic agents and insulin. She underwent sleeve gastrectomy with no post-operative complications. During the follow-up, she showed a steady reduction in her weight, along with maintaining normal blood sugars and pressure without medications. At 18 months of follow-up, IgAN remained in remission after stopping MMF at four months after the surgery. Obesity is considered an important cofactor in the progression of IgAN. This case highlights the importance of weight reduction to halt the progression of the disease.

How to cite this article:
Tiwari V, Gupta A, Arora V, Gupta P, John S, Divyaveer S, Bhargava V, Malik M, Gupta A, Bhalla AK, Rana DS. Clinical Remission of Immunoglobulin A Nephropathy after Bariatric Surgery in a Young Morbidly Obese Patient. Saudi J Kidney Dis Transpl 2021;32:1813-9

How to cite this URL:
Tiwari V, Gupta A, Arora V, Gupta P, John S, Divyaveer S, Bhargava V, Malik M, Gupta A, Bhalla AK, Rana DS. Clinical Remission of Immunoglobulin A Nephropathy after Bariatric Surgery in a Young Morbidly Obese Patient. Saudi J Kidney Dis Transpl [serial online] 2021 [cited 2023 Feb 4];32:1813-9. Available from: https://www.sjkdt.org/text.asp?2021/32/6/1813/352447

   Introduction Top

Obesity is the other end of the spectrum of malnutrition, which has engulfed the developed and developing nations alike. Such is its magnitude in terms of dissemination that the WHO calls it “Globesity” - the global epidemic of overweight and obesity.[1] In the US, the prevalence of obesity has been doubled over three decades, i.e., from 15% to 35% in 2011-2012.[2] In India, the situation is peculiar with the coexistence of obesity and undernutrition. Mostly rural India, it is the undernutrition that dominates, whereas due to a more sedentary lifestyle, better socioeconomic conditions, and higher caloric intake, urban India carries the other end of the spectrum. In a community-based survey by Sidhu et al, they found that the difference in the prevalence of urban and rural India is almost double (22% vs. 43.8%).[3]

Obesity and kidneys are intricately related to each other. All spectrum of renal disease can be found in obese patients. A cross-sectional study by Choung et al found that obesity-specific biopsy changes were found only in 30% of patients.[4] Seventy percent of patients had a full spectrum of kidney diseases, including acute tubular necrosis, glomerulonephritis, and chronic interstitial nephritis. Obesity has been linked to immunoglobulin A nephropathy (IgAN) in terms of rapid progression and poor outcome. Here, we described a case of a young, obese female with IgAN who achieved remission after undergoing bariatric surgery.

   Case Report Top

A 23-year-old female presented to the surgery clinic with morbid obesity [body mass index (BMI):41.8 kg/m2]. In the past, she was diagnosed to have IgAN (detailed renal biopsy report was unavailable) when she presented with gross hematuria, pedal swelling, normal renal function, and hypertension in 2007 (age: 11 years). Her BMI at that time was 25.6 kg/m2. She was started on steroids with angiotensin receptor blocker in view of nephrotic syndrome (24-h proteinuria - 7.1 g).She responded to the treatment but relapsed after three months after stopping steroids (course of six months). She was continued on steroids (10 mg/day) for four years, during which she developed diabetes mellitus [Figure 1] and obstructive sleep apnea. In view of severe metabolic syndrome, steroids were stopped, and mycophenolate mofetil (MMF) 1.5 g/day was started in 2011. In 2016, MMF was tapered and stopped, but she again presented two months later with nephrotic range proteinuria [urine polymerase chain reaction (PCR)- 4.9 g/g] with active sediments in urine with normal renal function. A repeat biopsy was done, which showed IgAN (M1E0S0T0C0) without any glomerulomegaly, focal segmental glomerulosclerosis (FSGS), or features of diabetic nephropathy [Figure 2]. Electron microscopy had electron-dense deposits in mesangium without any podocyte foot process effacement. She was reinitiated on MMF (2 g/day). In the next two months, her proteinuria decreased to subnephrotic range (urine PCR - 1.6 g/g). Her MMF was gradually tapered to 1.5 g/day and maintained at the same dose over the next two years till 2018.
Figure 1. The clinical course of the patient over 13 years.

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Figure 2. (a) Photomicrograph showing enlarged glomerulus with mesangial proliferation (H and E stain, 200× original magnification), (b) Photomicrograph showing granular mesangial IgA deposits (Immunofluorescence, 200× original magnification).

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She continued to put up on weight from 63 kg in 2007 to 104 kg in 2018. She had a history of binge eating with a preference for junk food. Multiple attempts at weight loss including sessions with dieticians, diet plans, and workout regimen had been unsuccessful. She had no family history of obesity or kidney disease.

In late 2018, in view of her morbid obesity and metabolic complications, she underwent laparoscopic sleeve gastrectomy [Table 1]. Postoperatively, she consistently lost weight from 106 kg preoperatively to 65 kg in 18 months of follow-up [Figures 3 and 4]. Over this period, her antihypertensive medication and oral hypoglycemics were withdrawn. At five months, her MMF was gradually tapered and stopped in view of normalization of urine protein and the disappearance of active sediments from the urine. At the last follow-up [Table 1], 1.5 years after the surgery, she was in remission with no proteinuria and bland urine sediments.
Table 1. Comparison of clinical and laboratory parameters at baseline and follow-up.
CRP: C-reactive protein, IL-6: Interleukin-6, RBC: Red blood cell.

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Figure 3. The trend of BMI and weight of the patient after the bariatric surgery.
BMI: Body mass index.

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Figure 4. The patient (a) before the surgery, (b) after 18 months postoperatively.

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The authors obtained all appropriate consent forms from the patient for the publication of this case report.

   Discussion Top

IgAN is the most common primary glomerulonephritis worldwide.[5] The major risk factors the progression of IgAN include age at presentation, degree of proteinuria, hypertension, and renal pathological findings.[5][6]

Obesity is an independent risk factor for deterioration of kidney function.[7],[8],[9] The impact of obesity on kidneys is not limited to structural integrity, but it also has various functional changes, including increased glomerular filtration rate, increased renal blood flow, and renal hypertrophy.[10],[11] Pathologically, it is seen as hypertrophied glomeruli with secondary FSGS. It is termed as obesity-related glomerulopathy (ORG).[12],[13]

Prognosis of ORG is poor, with 10%-33% of all patients developing progressive renal failure.[12],[14],[15] In general, patients with higher BMI (≥25.0 kg/m2) and body surface area (BSA) (≥1.73 m2) have significantly higher proteinuria in primary glomerulonephritis than the individuals with normal BMI and BSA.[16]

Since diabetes, ORG, hypertension, and IgAN can cause proteinuria independently, hence determining the etiology of proteinuria in the present case is not straightforward. First, there could be a possibility of superimposed ORG over the IgAN, which would explain the remarkable reduction of proteinuria postoperatively. In a meta-analysis including 24 studies with more than 2000 patients by Li et al, they found that there is a significant improvement in albuminuria and kidney function after bariatric surgery in patients with obesity.[17] However, our patient was biopsied three years before the surgery and did not reveal any features suggestive of ORG. In addition, microscopic hematuria on multiple occasions which subsided after the surgery points more in favor of remission IgAN than ORG. Second, the patient had an early onset of diabetes mellitus at the age of 13 years as a part of obesity, metabolic syndrome, and steroid use. Although the patient did not have evidence of diabetic retinopathy, her persistent proteinuria could have been explained by early diabetic nephropathy. Absence of micro- and macrovascular complications, paucity of mesangial expansion in renal biopsy, and response to the immunosuppressive drugs rule out the diabetic nephropathy. Third, her hypertension was well controlled throughout the period. Her renal biopsy as well as fundoscopy did not reveal any signs of uncontrolled hypertension.

Obesity and IgAN progression have been a matter of much debate.[6],[18],[19],[20],[21],[22],[23] Most studies have shown a direct correlation of BMI with IgAN progression.[19],[22],[23] In the study by Wu et al and Berthoux et al, authors have concluded that high BMI does not have an independent effect on the outcome of the disease.[20],[24] However, it was found that obese patients had more severe interstitial fibrosis at the presentation, along with other increased proteinuria, which could lead to more rapid progression and ESRD. The mechanism of progression of IgAN in obese individuals appears to be multifactorial including the related metabolic disorders, obesity-induced pathological changes, and renal injury caused by various hemodynamic and nonhemodynamic mechanisms of adipocytes [Figure 5].[12],[19],[25],[26],[27],[28] All the previous studies which have specifically studied the effects of obesity on IgAN have included patients with mild obesity [Table 2]. Mechanisms that operate on the kidney with IgAN with morbid obesity are yet to be identified.
Figure 5. Relationship between IgA nephropathy and obesity.
IgA: Immunoglobulin A.

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Chronic inflammation is a constant feature of obesity and involves abnormal cytokines and activation of pro-inflammatory pathways.[29] Adipocytes are source of numerous endocrine and immunological mediators rather than just mere fat-storing cells. The term “Metainflammation” has been coined to describe the metabolically triggered inflammation apparent in obesity due to high levels of inflammatory markers such as IL-1, IL-6, and TNF-alpha.[30]

The significant weight loss achieved in this case might have led to the abatement of “metainflammation” i.e. toning down the inflammation and thus removing the additional insult on the kidneys that is present along with IgAN.

In a case reported by Soto et al, a morbidly obese patient was incidentally found to have renal dysfunction (creatinine − 9.9 mg/dL, hematuria, and proteinuria) while being evaluated for bariatric surgery. Although renal biopsy lacked immunofluorescence, light microscopy and clinical presentation were highly suggestive of IgAN without any ORG. By the 7th month postoperatively, his renal function (creatinine − 1.6 mg/dL) recovered drastically.[31]

Obesity acts like a fertile soil where weeds of hypertension, diabetes, and metabolic syndrome flourish and gradually overtake the normal vegetation. Timely intervention in the form of a healthy diet, exercises, behavioral therapy, and bariatric surgery can prevent these complications before the irreversible damage happens.

   Conclusion Top

Obesity is a risk factor for progressive renal damage. IgAN with obesity poses a higher risk for progression of disease including difficult to achieve remission. A successful and sustained weight loss in morbidly obese patients can aid the attainment of remission. Correction of morbid obesity may not just halt further progression of IgAN but also induce remission.

Conflict of interest: declared.

   References Top

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Choung HG, Bomback AS, Stokes MB, et al. The spectrum of kidney biopsy findings in patients with morbid obesity. Kidney Int 2019;95:647-54.  Back to cited text no. 4
Barratt J, Feehally J. IgA nephropathy. J Am Soc Nephrol 2005;16:2088-97.  Back to cited text no. 5
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Correspondence Address:
Vaibhav Tiwari
Department of Nephrology, Sir Ganga Ram Hospital, New Delhi, India.
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1319-2442.352447

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]

  [Table 1], [Table 2]


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