Saudi Journal of Kidney Diseases and Transplantation

: 2009  |  Volume : 20  |  Issue : 1  |  Page : 116--119

Minimal change disease versus IgA nephropathy

Wael Latif Jabur 
 Nephrology Section, New Medical Center Specialty Hospital, Dubai, United Arab Emirates

Correspondence Address:
Wael Latif Jabur
Specialist Nephrologist, NMC Specialty Hospital, P.O. Box 7832, Dubai
United Arab Emirates


IgA nephropathy is the most common type of the glomerulonephritis all over the world. However, its clinical presentation is variable, as is the underlying histopathological lesion. We report herein a case of an adult with steroid responsive minimal change disease and IgA mesangial deposits. During the first two weeks of therapy with prednisolone, the patient reported dramatic improvement in his clinical condition and remitted his disease. Unfortunately, at the end of the second month of prednisolone therapy, an acute flare of viral hepatitis was diagnosed. Interes­tingly, the acute viral flare was without a concomitant relapse of proteinuria.

How to cite this article:
Jabur WL. Minimal change disease versus IgA nephropathy.Saudi J Kidney Dis Transpl 2009;20:116-119

How to cite this URL:
Jabur WL. Minimal change disease versus IgA nephropathy. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2023 Jan 29 ];20:116-119
Available from:

Full Text


IgA nephropathy is the most common type of the glomerulonephritis all over the world. How­ever, its clinical presentation is variable, as is the underlying histopathological lesion. Abnor­mality of the IgA immunoglobuline molecule is widely blamed as the main culprit in its patho­genesis, and this hypothesis is the hub for a plenty of researches. Nephrotic syndrome is widely recognized in IgA nephropathy.

We report herein a case of steroid responsive minimal change disease and IgA mesangial de­posits.

 Case Report

A 53-year-old man of African origin presented with a recent history of nephrotic syndrome, hypertension, and renal impairment. The past medical history was unremarkable for hema­turia, proteinuria, hypertension, and diabetes. Drug history was negative.

On examination, the patient was hypervolemic and hypertensive with blood pressure of 180/100, otherwise unremarkable for other cli­nical findings.

Laboratory investigations revealed 24-hour pro­teinuria of 4 grams, no active urine sediment, serum creatinine of 1.7mg/dL, serum albumin of 2 gm/dL, normal complement system levels, negative antinuclear antibodies (ANA), negative anti-nuclear cytoplasmic antibodies (ANCA), and negative paraproteinemia assays. Virology screening he was positive for hepatitis B viral antigen (HBsAg) without evidence of active replication (viral copies were less than 100,000/ mL and HBeAg was negative) and the serum transaminases were normal. We did not check for viral genotype. The rest of investigations were unremarkable.

Kidney biopsy was performed after controlling blood pressure and volume status. Hematoxylin and Eosin light microscopy examination re­vealed normal capillary loops mild focal in­crease of the mesangial cells, and no extra capillary proliferation. Periodic Acid Schiff staining revealed mild diffuse mesangial matrix accentuation and the silver staining showed nor­mal capillary walls, while the Congo red stai­ning for amyloidosis was negative. Similarly, the Mason trichrome staining showed normal tubules and interstitium. Immunoflourescent study was strongly positive for IgA, IgG and C3 com­plement in the mesangium and the capillary walls. Electron microscopy spotted the presence of dense deposits in the mesangium [Figure 1] and the subendothelial area [Figure 2], with mild mesangial expansion and diffuse foot processes effacement and focally thinning of otherwise intact basement membrane. There was no evi­dence of intracellular inclusion bodies.

A diagnosis of IgA nephropathy associated minimal change disease was suggested and a therapeutic regimen consisted of prednisolon of 1 mg/kg body weight, a loop diuretic, calcium 500 twice daily, resuvastatin 5 mg/day, and multi­vitamins was initiated. The patient was followed weekly as an outpatient to check for urine pro­tein, blood pressure, and for probable complica­tions of the therapy.

During the first two weeks of therapy, the patient reported dramatic improvement in his clinical condition, and at the end of the third week the urine was protein free, serum albumin was 3.7 mg/dL, and serum creatinine was 1.0 mg/dL. The prednisolone dose was maintained till the end of the second month and then ta­pered to 40 mg every other day. Unfortunately, at the end of the second month an acute flare of viral hepatitis was diagnosed, with a viral load of 400,000 copies/mL, and three folds elevation of the transaminases. Accordingly, an antiviral protocol consisted of Adivofir 10 mg/day was started. Interestingly, the acute viral flare was without a concomitant relapse of protienuria.


The clinical presentation and the rapid remi­ssion of the nephrotic syndrome on predniso­lone are consistent with minimal change disease (MCD). Despite the fact that the association of minimal change disease and IgA nephropathy is well known, it is very rarely if ever reported to my knowledge the solely presentation of MCD with IgA nephropathy as the nephrotic syn­drome without hematuria. [1],[2],[3]

Mesangial IgA deposits are the defining hallmark of IgA nephropathy accompanied by com­plement C3 and some times IgG deposition, with variable histopathological patterns. Accor­ding to Lee and Haas classification, [4] our patient has stage 1 IgA nephropathy. The common pre­sentation of such a patient should be macros­copic and microscopic hematuria with variable degree of proteinuria. However, it is not un­common to find a patient with significant histo­logical damage despite the absence of clinical risk factors. [4]

It is very rare for proteinuria to occur without microscopic hematuria in IgA nephropathy, and the nephrotic syndrome was reported to occur in 5% of the patients during the course of IgA nephropathy. [5]

IgA nephropathy might be associated with the nephrotic syndrome at any stage of the disease and it is probably attributable to a concomitant minimal change nephropathy in the early stages and to mesangial sclerosis and crescentic glo­merulonephritis in the advanced stages. [6]

Despite the fact that the IgA immunoglobulin deposits in the capillary walls in addition to the mesangial deposits are usually associated with a poor prognosis, [5],[7] our patient's nephrotic syn­drome was sensitive to steroid and his short term prognosis was very good, in contrast to some previous reports that showed more slower response to the steroid therapy. [1]

The hallmark of the MCD is the normal histo­logy on light microscopy, absence of the immu­noglobulins on immunoflourescent study, and characteristically diffuse foot processes efface­ment on electron microscopic examination. Se­veral variants of MCD are well recognized that include mesangial hypercellular, IgM nephro­pathy, and C1q nephropathy. [8],[9] Many authors recognize the variants of MCD as different di­seases and have considered their clinical beha­vior more consistent with idiopathic focal seg­mental glomerulosclerosis (FSGS) than MCD, which is not the case in our patient. [10]

Mesangial expansion and hypercellularity are a nonspecific response to injury, which might be mediated by up-regulation and secretion of tissue growth factor (TGFI3), such as the depo­sition of immune-complexes, immunoglobulins, and complement, [5] or it might be idiopathic as in mesangial proliferative variant of MCD. In our case, we could not consider the mesangial pro­liferation as an idiopathic variant due to the pre­sence of a significant mesangial IgA deposits. The presence of IgA mesangial and capillary deposits in the context of the nephrotic syn­drome and negative urine sediment might repre­sent more an early asymptomatic (Lanthanic) IgA nephropathy [11] with a concomitant minimal change disease. On the other hand, the lack of the urinary active sediment and the dramatic response to the steroid may be explained by a new variant of MCD. The response to therapy with steroids is more consistent with MCD than FSGS.

The etiology of acute renal failure that ob­served in adult MCD is usually due to acute tubular necrosis in severe cases, otherwise mild renal failure reported in hypervolemic patients is usually due to renal interstitial edema, which most probably was the case in the index patient because of the rapid and marked improvement with therapy.

The patient flare of the viral hepatitis high­lights the debate of administering prophylactic antiviral therapy for the patients who are ca­rriers of the hepatitis virus, [12],[13] while they are maintained on long-term steroid therapy. This is in agreement with Oren Shibolet et al study, which recommended the use of prophylactic antiviral therapy for any patient who is a HBV carrier (with or without active viral replication) while undergoing immunosuppressive protocol. [13] Because of the current remission of the nephro­tic syndrome in the face of relapse of active viral hepatitis, we may conclude that the viral hepatitis infection was not temporally related to the pathogenesis of IgA or minimal change disease.


1Cyclosporin A therapy in frequently relapsing nephrotic syndrome and IgA nephropathy. Nephrol Dial Transplant 1997;12(11):2402-4.
2Nator SN, Strom JA, Occi A. Relapsing neph­rotic syndrom in a patient with Kimura s disease and IgA nephropathy. Nephrol Dial Transplant 1998;13(9):2358-63.
3Boix E, Rivera F, Gil CM, Perez-Contreras J, Olivares J. Nephrotic syndrome with minimal change disease and IgA deposits in a HIV­infected patient. Nephrol Dial Transplant 2000; 15(3):412-4.
4Li PK, Ho KK, Szeto CC, Yu L, Lai FM. Prognostic indications of IgA nephropathy in the Chinese-clinical and pathological perspective. Nephrol Dial Transplant 2002;17(1):64-9.
5Barratt J, Feehally J. IgA nephropathy. J Am Soc Nephrol 2005;16(7):2088-97.
6Tumlin JA, Lohavichan V, Hennigar R. Cres­centic, proliferative IgA nephropathy: Clinica and histological response to methylprednisolon and intra-venouse cyclophosphamide. Nephrol Dial Transplant 2003;18(7):1321-9.
7Tumlin JA, Mdaio MP, Hennigar R. Idiopathic IgA Nephropathy: Pathogenesis and therapeutic options. J Am Soc Nephrol 2007;18(5):1054-61.
8Waldman M, Crew RJ, Valeri A, et al. Adult minimal change disease: Clinical characteris­tics, treatment and outcome. Clin J Am Soc Nephrol 2007;2(3):445-53.
9Howie AJ. Pathology of minimal change disease and segmental sclerosing glomerular disorders. Nephrol Dial Transplant 2003;18 (Suppl 6):VI33-8.
10Alexopoulos E, Papagranni A, Stangon M, Pantzaki A, Papadimitriou M. Adult onset idio­pathic nephrotic syndrom associated with diffuse mesangeal hypercellularity. Nephrol Dial Transplant 2000;15(7):981-7.
11Suzuki K, Honda K, Tanabe K, Toma H, Nihei H, Yamaguchi Y. Incidence of latent mesangial IgA deposition in renal allograft donors in Japan. Kidney Int 2003;63(6):2286-94.
12Tsou PL, Lee HS, Jeng YM, Huang TS. Submassive liver necrosis in a hepatitis B carrier with cushing syndrom. J Formos Med Assoc 2002;101(2):156-8.
13Shibolet O, Ilan Y, Gillis S, Hubert A, Shouval D, Safadi R. Lamivudin therapy for prevention of immunosuppressive-induced hepatitis B virus reactivation in HBs Antigen carriers. Blood 2002;100(2):391-6.