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 Table of Contents  
ORIGINAL ARTICLE
Year : 2014  |  Volume : 28  |  Issue : 3  |  Page : 180-184

Clinicopathological correlation in primary nephrotic syndrome


1 Department of Medicine, Jawaharlal Nehru Institute of Medical Sciences Hospital, International School and Junior College, Regional Institute of Medical Sciences, Imphal, Manipur, India
2 Department of Medicine, International School and Junior College, Regional Institute of Medical Sciences, Imphal, Manipur, India
3 Department of 2Pathology, International School and Junior College, Regional Institute of Medical Sciences, Imphal, Manipur, India

Date of Web Publication5-Jan-2015

Correspondence Address:
Ghanachandra K Singh
Department of Medicine Jawaharlal Nehru Institute of Medical Sciences Hospital, Porompat, Imphal - 795 001, Manipur
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0972-4958.148517

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  Abstract 

Objective: To study the clinicopathological correlation in patients suffering from primary/idiopathic nephrotic syndrome. Materials and Methods: A total of 34 cases of idiopathic nephrotic syndrome were included in the present study. All patients had undergone renals biopsy for histological diagnosis. Results: The patients were subjected to renal biopsy and on the basis of light microscopic findings they were divided into two broad groups. Group A included 25 patients whose renal biopsy showed histological picture of minimal change disease. Group B included nine patients whose renal biopsy showed features other than those seen in minimal change disease. Most patients presented in the 2 nd and 3 rd decade (range was found from 14 to 80 years). Increased serum creatinine (<1.6 mg%) wasfound in two (8%) in group A and four (44%) in group B. Thus, the number of patients having high serum creatinine was significantly higher in group B. Nine patients (33%) in group A and three (33%) in group B had low glomerular filtration rate (GFR;i.e.,<90m1/min). Low serum protein (i.e.,<6 g%) was seen in 18(72%) in group A and five (55.5%) in group B and low serum albumin (i.e.,< 3.2 g%) was found in 21 (84%) in group A and six (66%) in group B. The mean serum cholesterol was 426.76 ΁ 77.11 mg% and mean triglyceride was 269.80 ΁ 148.11 mg% in group A, while in group B the mean cholesterol was 357.33 ΁ 116.19 mg% and mean serum triglyceride was 231.55 ΁ 73.85 mg%. Conclusion: Most patients of nephrotic syndrome presented in the 2 nd and 3 rd decades. All patients in both the groups had high serum triglycerides. Seventy-three percent of nephrotic syndrome cases had histopathological diagnosis of minimal change disease, 8.8% had membranoproliferative glomerulonephritis. Membranous glomerulonephritis, focal segmented glomerulosclerosis, and diffuse proliferative glomerulonephritis accounted for 6% cases each.

Keywords: Glomerular filtration rate, glomerulonephritis, nephrotic syndrome


How to cite this article:
Singh GK, Singh SN, Niroula D, Singh lY, Debnath K, Sharma RL. Clinicopathological correlation in primary nephrotic syndrome. J Med Soc 2014;28:180-4

How to cite this URL:
Singh GK, Singh SN, Niroula D, Singh lY, Debnath K, Sharma RL. Clinicopathological correlation in primary nephrotic syndrome. J Med Soc [serial online] 2014 [cited 2020 Oct 22];28:180-4. Available from: https://www.jmedsoc.org/text.asp?2014/28/3/180/148517


  Introduction Top


The nephrotic syndrome is a clinical syndrome complex characterized by a number of renal and extrarenal features, the most prominent of which are proteinuria >3.5g/1.73m 3 /24 h (in practice >3.0-3.5 g/24 h), hyperlipidemia, lipiduria, and hypercoagu1abi1ity. [1] The underlying cause of most glomerular diseases producing nephrotic syndrome remains an enigma. Infectious agents, autoimmunity, drugs, inherited disorders, and environmental agents have been implicated as the causes. Glomerular diseases may be categorized into those that primarily involve the kidney (primary glomerular disease), for example, primary nephrotic syndrome and those in which kidney involvement is a part of systemic disorder (i.e., secondary glomerular disease [2] ). Proteinuria, results from altered permeability of the glomerular filtration barrier for protein, namely glomerular basement membrane (GBM), podocytes, and their slit diaphragm. The other components of the nephrotic syndrome and the ensuing metabolic complications are secondary to urinary protein loss. Edema is the most common presenting symptom. Hypovolemia as aconsequence of reduced plasma oncotic pressure has been long considered the principal cause of salt and water retention by kidneys, along with activation of rennin-angiotensin-aldosterone, sympathetic nervous, and vasopressin systems. Hyperlipidemia is one of the salient features of nephrotic syndrome, patients developed numerous alternations in lipid profile includinghypercholesterolemia and hypertriglyceridemia. Hyperlipidemia is thought to be the consequence of both increased hepatic lipoprotein synthesis and decreased catabolism. Many types of glomerular lesions are associated with nephrotic syndrome. These are minimal change glomerulopathy, membranous glomerulopathy, focal segmentalglomerulosclerosis, mesangioproliferative glomerulopathy, and diffuse proliferative glomerulopathy.

The most important of the primary glomerular lesions that characteristically lead to nephrotic syndrome are membranous glomerulonephritis and minimal change diseases. The incidence of nephrotic syndrome is quite high in Manipur, but so far no clinicopathological correlation has been attempted among patients with nephrotic syndrome. So the present study was planned to study the clinicopathological correlation in primary nephrotic syndrome patients attending Regional Institute of Medical Sciences Hospital, Imphal, Manipur.


  Materials And Methods Top


The present study was undertaken at the Department of Medicine, Regional Institute of Medical Sciences, Imphal, Manipur, between September 2004 and August 2006. A total number of 34 cases of idiopathic nephrotic syndrome were included in the present study irrespective of age and sex. Selection of patients; inclusion criteria:



  1. a. All patients of primary nephrotic syndrome willing for renal biopsy and






Diagnostic criteria for primary nephrotic syndrome:



  1. a. 24 h urinary protein >3.5 g/1.732 m 2 /24 h and






Exclusion criteria: Diabetes, renal failure, secondary causes of nephrotic syndrome, and urinary tract infection. A detailed history was taken for each patients to ascertain past and present illness. All the patients were subjected to detailed clinical examination to detect involvement of the heart, lungs, and other organs. Height and weight were taken and body mass index (BMI) was calculated. The following investigation were carried out:



  1. a. Random blood sugar (RBS),
  2. b. Blood urea and creatinine,
  3. c. Glomerular filtration rate (GFR; i.e., ml/mm = ((140- age) × body weight/serum Creatinine × 72) (in female × 0.85)),
  4. d. Serum electrolytes,
  5. e. Lipid profile,
  6. f. X-ray for kidney, ureter, and bladder (KUB) region,
  7. g. Computed tomography (CT) scan abdomen (when indicated), and






All the patients were subjected to renal biopsy using Tru-Cut kidney biopsy needle. The biopsy specimen was processed and stained routinely with hematoxylin and eosin. Special stains were used when required. Collection of urine sample for 24 h was done and quantitative analysis of protein in 24 h was done using turbidity method.

The principal of method is thatthe proteins are denatured by action of acids. Due to denaturation, the specific internal structure of the protein is changed to an insoluble form, which is exhibited by the formation of a turbid solution; 24 h urinary protein = urinary protein ΄ 24 h urine volume in dl.


  Results Top


The patients were divided into two groups: Group A and B. Group A included patients whose renal biopsy showed histopathological picture of minimal change disease. There were 25 patients in this group.

Group B included patient whose renal biopsy showed features other than those seen in minimal change disease. There were nine patients in this group. Age distribution of the patients; most of the patients presented in the 2 nd and 3 rd decade. In group A, the commonest age group was 21-30 years with a mean of 26.08 ± 11.45 years. In group B, the commonest age group was 11-20 years with a mean of 30.55 ± 20.77 years [Table 1]. The presenting symptoms are shown in [Table 2].
Table 1: Age distribution


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Table 2: The presenting symptoms


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Blood pressure (BP)

The number of patients having hypertension (i.e., BP >40/90 mmHg) was one (4%) in group A and four (44.4%) in group B, the incidence of hypertension was significantly higher in group B (P = 0.041).

BMI

In group A, the mean BMI was 17.56 ± 1.76 and in group B the mean BMI was 16.02 ± 18.5. The number of patients having low BMI (i.e., BMI <18) were 14 (50%) in group A and 5 (55%) in group B.

Blood urea

In group A, the mean blood urea was 29.60 ± 13.42 mg% and in group B, the mean was 48.11 ± 21.04 mg%. The number of patients having high blood urea (i.e., >40 mg%) were six (24%) in group A and six (66.6%) in group B. The blood urea was significantly higher in group B (P = 0.0170). Serum creatinine; in group A the mean serum creatinine was 1.03 ± 0.44 mg% and group B it was 1.52 ± 0.54 mg%. The difference was significant (P = 0.0112). The number of patients having high serum creatinine (i.e., >1.6 mg/dl) were two (8%) in group A and four (44.4%) in group B. Thus, the number of patients having high serum creatinine was significantly higher in group B (P = 0.0400). GFR: The mean GFR in group A was 93 ± 1.55 ml/min and 90 ± 0.65 ml/min in group B. The number of patients having low GFR (i.e., <90 ml/min) were nine (36%) in group A and three (33.3%) in group B, the difference was statistically insignificant (P = 0.186). Serum protein: The mean serum protein was 5.28 ± 1.04 g% in group B. There is no variation in serum proteins between the two groups (P = 0.453). The number of patient having low serum protein (i.e.,<6 g%) were 18 (72%) in group A and five (55.5%) in group B. Statistically the difference was insignificant (P = 0.262).

Serum albumin

The mean serum albumin was 2.45 ± 0.75 g% in group A and 85 g% in group B. The number of cases haying low serum albumin (i.e.<3.2 g) were 21 (84%) in group A and six (66%) in group B. This difference was statistically insignificant (P = 0.331). Lipid profile: In group A, the mean serum cholesterol was 426.76 ± 177.11 mg% and 357.33 ± 116.19 mg% in group B. The number of patients having high serum triglyceride (i.e., >150 mg%) were 25 (100%) in group A and nine (100%) in group B. 24 h urinary protein excretion: The mean 24 h urinary protein excretion was 5.32 g/day in group A and 5.76 ± 2.75 in group B. There was no significant difference between the two groups (P = 0.580) [Table 1].{Table 1}

Histopathological diagnosis

In order to properly evaluate morphology and periodic acid-Schiff (PAS) stained section of 2.3 microns were studied under different compartment, for example, glomeruli, tubules, and interstitium with vascular change [Figure 1]. Twenty-five patients (73.5%) in our series were characterized by absence of pathological changes by light microscopy and were diagnosed as minimal change glomerulonephritis and three cases (8%) revealed large and hypercellular glomeruli [Figure 2] and [Figure 3] with thickened GBM depicting "tram-track" appearance on PAS stain [Figure 4] and were diagnosed as membranoproliferative glomerulonephritis. There were variable amounts of interstitial fibrosis and tubular atrophy, but no obvious interstitial cellular infiltrate. The cases were diagnosed as membranous glomerulonephritis.
Figure 1 : Microphotograph showing normal glomerulus (periodic acid- Schiff (PAS) stain, ×40)

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Figure 2 : Photomicrograph showing mesangial hypercellularity with endocapillary proliferation (hematoxylin and eosin (H and E) stain, × 40)

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Figure 3 : Photomicrograph showing normocellular glomerulus (H and E stain, × 40)

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Figure 4 : Photomicrograph showing glomerulus with thicken basement (H and E stain, × 40)

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Two patients (5.9%) revealed focal segmental obliteration of glomerular capillaries, tubular atrophy, and interstitial fibrosis. Blood vessels were apparently normal. The cases were diagnosed as focal segmental glomerulosclerosis and two cases (5.9%) had diffuse glomerulonephritis. There were no other associated disease processes in both the cases [Table 3].
Table 3: Histopathology of renal biopsy


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  Discussion Top


The most common primary glomerular diseases causing nephrotic syndrome in children and adults are minimal change diseases and membranous glomerulonephritis, respectively. [3] However, recent reports suggest a changing trend in the etiology of primary nephrotic syndrome. Focal segmental glomerulosclerosis is most common cause of primary nephrotic syndrome in children and adults. [4] The severity of proteinuria is strong independent risk factors for the prognosis of renal diseases. Control of proteinuria is therefore essential to prevent the progression of renal diseases to chronic renal failure. [5] Establishing the type of glomerular diseases is essential from the therapeutic point of view and for predicting the prognosis. Therefore, renal biopsy should be performed particularly in adult patients of nephrotic syndrome. In our study, minimal change diseases occurred mostly in the younger age group when compared to the other causes of primary nephrotic syndrome. This finding is consistent with the findings of other workers. [6],[7] In this study, we observed that edema was the most common presenting symptom in patients of nephrotic syndrome, which is also reported by another study. [2] Another study of pathophysiology of nephrotic syndrome described that the most notable consequence of massive continuous proteinuria is the expansion of the body water by as much as 100% leading to edema. [8] Clinical presentations of older patients with minimal change nephrotic syndrome as it was reported by another study were similar to those of younger patients which is also observed in our study. [9] In our series we find that hypertension is less common in minimal change diseases when compared to other histopathological types. This finding is consistent with findings of other study reported. [8] From the study of BMI of the patients of nephrotic syndrome, we concluded that most patients of nephrotic syndrome were undernourished. It was also reported that rising blood urea reflected renal insufficiency. [10] The creatinine was significantly higher in group B patients in our study. Another study reported that in nephrotic syndrome renal function was usually normal, although serum creatinine might be slightly increased at the time of presentation. Twelve patients had diminished GFR (i.e.,<90 ml/min). This finding predicts the tendency of patients to progress towards renal insufficiency. Hyperlipidemia is also often present in nephrotic syndrome. [11] Total cholesterol may be increased 10-fold. Hypertriglyceridemia may be present, but is usually less severe as we find in our finding. We also detected that the 24 h urinary protein excretion ranged from 3.5 to 10.8 g/day. Another study suggested that the rate of progression of variety of renal pathological conditions is related to the state of proteinuria, it was also predicted that heavy proteinuria was the worst prognostic marker and among the causes of nephrotic syndrome, [5],[12] membranoproliferative glomerulonephritis is the commonest cause of nephrotic syndrome.

In conclusion,nephrotic syndrome occurs commonest in the 2 nd and 3 rd decades in our study. The most common cause of primary nephrotic syndrome is minimal change diseases, edema being the commonest presenting sign. Many cases are associated with reduced GFR, low serum proteins and albumin levels, hyperlipidemia, and heavy proteinuria. Renal biopsy is therefore essential to establish the histopathological diagnosis of nephrotic syndrome.

 
  References Top

1.
Brady HR, Brenner BM, O'Meara YM. Glomerular diseases. In: Fauci AS, Braumwal E, Kasper DL, Langol DL, Jameson JL, editors. Harrison's Principles of Internal Medicine. 16 th ed., vol. 2. New York: Mc Graw Hill; 2004. p. 1674-94.  Back to cited text no. 1
    
2.
Falk RJ. Jennettee JC, Nachman PH. Primary Glomerular diseases. The Kidney Brenner and Rector's. 7 th ed. Philadelphia: Saunders; 2004. p. 1293-382.  Back to cited text no. 2
    
3.
Broyer M, Meyrier A, Naiduet P. Minimal changes and focal segmental glomerulosclerosis. In: Davidson AM, Cameron JS, Grunfeld JP, Kerr NS, Ritz E, Winearls CG. Editors. Oxford textbook of clinical nephrology. 2 nd ed., vol.1. London: Oxford University press; 1988. p. 493-535.  Back to cited text no. 3
    
4.
Cameron JS, Turner DR, Ogg CS, Chantler C, Williams DS. The long term prognosis of patients with focal segmental glomerulosclerosis. Clin Nephrol 1978;10:213-8.  Back to cited text no. 4
    
5.
Burton C, Harris KP. The role of proteinuria in the progression of chronic renal failure. Am J Kidney Dis 1996;27:765-75.  Back to cited text no. 5
    
6.
Glassok RJ, Cohen AH, Adler SG. Primary glomerular diseases. In: Brenner BM, editor. The Kidney. 5 th ed., vol. 2. Philadelphia: Saunders; 1996. p. 1396-2012.  Back to cited text no. 6
    
7.
Tuner AN, Savill J, Setwart LH, Cumming. Principles and practice of Medicine. In: Haslett A, Chilvers ER, Boon NA, Cooedge NR, editors. 19 th ed. London. 2004. p. 575-639.  Back to cited text no. 7
    
8.
Cameron JS, Glassock RJ. The nephrotic syndrome. In: Dekker M, editor. 5 th ed. New York. 1988. p. 561-80.  Back to cited text no. 8
    
9.
Tse KC, Lam MF, Yip PS, Lio FK, Chou BY, Lai KN, et al. Idiopathic minimal change nephrotic syndrome in adults: Steroid responsiveness and patterns of relapses. Nephrol Dial Transplant 2003;18:1316-20.  Back to cited text no. 9
    
10.
Charles EA. The kidney Robbins Cotran Pathologic basis of diseases. In: Kumar V, Abbs AK, Fausto N, editors. 7th ed. New Delhi: Elsevier; 2004. p. 955-1021.  Back to cited text no. 10
    
11.
Keane WF, Kasiske BI, O Donnel MP. Lipids and progressive glomerulosclerosis. Am J Nephrol 1998;8:262-71.  Back to cited text no. 11
    
12.
Klahr S, Levey AS, Beck GJ, Caggiula AW, Hunsicker L, Kusek JW, et al. The effects of dietary protein restriction and blood pressure control on the progression of chronic renal diseases. Modification of Diet in Renal Disease Study Group. N Engl J Med 1994;330:877-84.  Back to cited text no. 12
    


    Figures

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

  [Table 1], [Table 2], [Table 3]



 

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