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Currently there is growing evidence that obesity may cause silent but
severe damage to the kidneys in some otherwise healthy individuals [1-5].
Raised intra-abdominal pressure and likely changes in intrarenal
hemodynamic forces caused by medullary compression due to accumulation of
adipose tissue around the kidney and increased extracellular matrix within
the kidney has been reported to be related to obesity associated
hypertension [2]. In addition, enhanced tubular reabsorption of sodium-
closely linked to activation of the sympathetic and renin-angiotensin
systems, may also be involved in the pathogenesis of obesity-induced
hypertension.
An initial increased glomerular blood flow and glomerular filtration
rate (GFR) culminating in to renal hypertrophy and hyperfiltration
glomerular injury complicated subsequently by microalbuminuria, has been
well described in obesity [2]. While a graded, positive increase in
prevalence of microalbuminuria across quintiles of waist-to-hip ratio was
observed in non-hypertensive subjects in MONICA Augsburg survey during
1994-95; microalbuminuria was consistently high among the subjects with
hypertension and central obesity [3].
A study of 6818 native renal biopsies reviewed from 1986 to 2000
revealed a progressive significant increase in biopsy incidence of Obesity
associated focal segmental glomerulosclerosis (Ob-FSGS) from 0.2% in 1986-
1990 to 2.0% in 1996-2000 [4]. Distinct clinico-pathological features such
as, FSGS lesions with glomerulomegaly (with dilatation of glomerular
diameter due to glomerular loop elongation), less severe foot process
effacement, absence of features of nephrotic syndrome despite nephrotic-
range of proteinuria, are helpful in differentiating this entity from
idiopathic FSGS. Ob-FSGS is an indicator of poor prognosis with nearly 50%
patients developing advanced renal failure [4]
In a recent study involving 162 patients with biopsy-proven primary
IgA nephropathy, an elevated body mass index (BMI) of more than 25 kg/m2
was found to be an independent risk factor for the development of systemic
hypertension and clinical and pathological progression to end stage renal
disease (ESRD) [5]. In addition several studies have shown that obese
individuals carry a substantially elevated risk of development of renal
cell carcinoma.
Thus, obesity possibly provokes a metabolic syndrome of insulin
resistance which results in the dysregulation of hemodynamic and oxidative
stress factors with resultant endothelial dysfunction, and eventually
glomerulosclerosis. Preliminary data suggests that antioxidant therapy
with a-tocopherol, ascorbic acid and a-carotene, may be valuable in the
regeneration of cytoprotective enzymes and the restoration of endothelial
function in obesity associated renal disease.
References
1.Manuel P. Obesity a neglected culprit in renal disease. Nephrol
Dial Transplant. 2002; 17: 1157-59.
2.Sugerman HJ. Effects of increased intra-abdominal pressure in
severe obesity. Surg Clin North Am 2001; 81:1063-75.
3.Liese AD, Hense HW, Doring A, Stieber J, Keil U. Microalbuminuria,
central adiposity and hypertension in the non-diabetic urban population of
the MONICA Augsburg survey 1994/95. J Hum Hypertens 2001; 15:799-804.
4.Praga M, Hernandez E, Morales E et al. Clinical features and long-
term outcome of obesity-associated focal segmental glomerulosclerosis.
Nephrol Dial Transplant 2001; 9:1790-98.
5.Bonnet F, Deprele C, Sassolas A et al. Excessive body weight as a
new independent risk factor for clinical and pathological progression in
primary IgA nephritis. Am J Kidney Dis 2001; 37:720-27.
Competing interests:
None declared
Competing interests:
No competing interests
12 May 2003
ANIL K. SAXENA, MD; MRCP (Dublin)
Consultant Nephrologist & Deputy Chief
Nephrology Division, King Fahad Hospital & Tertiary care Center, Hofuf, Al-Hasa-31982, Saudi Arabia
Renal repercussions of an emerging global “epidemic” of obesity
Currently there is growing evidence that obesity may cause silent but
severe damage to the kidneys in some otherwise healthy individuals [1-5].
Raised intra-abdominal pressure and likely changes in intrarenal
hemodynamic forces caused by medullary compression due to accumulation of
adipose tissue around the kidney and increased extracellular matrix within
the kidney has been reported to be related to obesity associated
hypertension [2]. In addition, enhanced tubular reabsorption of sodium-
closely linked to activation of the sympathetic and renin-angiotensin
systems, may also be involved in the pathogenesis of obesity-induced
hypertension.
An initial increased glomerular blood flow and glomerular filtration
rate (GFR) culminating in to renal hypertrophy and hyperfiltration
glomerular injury complicated subsequently by microalbuminuria, has been
well described in obesity [2]. While a graded, positive increase in
prevalence of microalbuminuria across quintiles of waist-to-hip ratio was
observed in non-hypertensive subjects in MONICA Augsburg survey during
1994-95; microalbuminuria was consistently high among the subjects with
hypertension and central obesity [3].
A study of 6818 native renal biopsies reviewed from 1986 to 2000
revealed a progressive significant increase in biopsy incidence of Obesity
associated focal segmental glomerulosclerosis (Ob-FSGS) from 0.2% in 1986-
1990 to 2.0% in 1996-2000 [4]. Distinct clinico-pathological features such
as, FSGS lesions with glomerulomegaly (with dilatation of glomerular
diameter due to glomerular loop elongation), less severe foot process
effacement, absence of features of nephrotic syndrome despite nephrotic-
range of proteinuria, are helpful in differentiating this entity from
idiopathic FSGS. Ob-FSGS is an indicator of poor prognosis with nearly 50%
patients developing advanced renal failure [4]
In a recent study involving 162 patients with biopsy-proven primary
IgA nephropathy, an elevated body mass index (BMI) of more than 25 kg/m2
was found to be an independent risk factor for the development of systemic
hypertension and clinical and pathological progression to end stage renal
disease (ESRD) [5]. In addition several studies have shown that obese
individuals carry a substantially elevated risk of development of renal
cell carcinoma.
Thus, obesity possibly provokes a metabolic syndrome of insulin
resistance which results in the dysregulation of hemodynamic and oxidative
stress factors with resultant endothelial dysfunction, and eventually
glomerulosclerosis. Preliminary data suggests that antioxidant therapy
with a-tocopherol, ascorbic acid and a-carotene, may be valuable in the
regeneration of cytoprotective enzymes and the restoration of endothelial
function in obesity associated renal disease.
References
1.Manuel P. Obesity a neglected culprit in renal disease. Nephrol
Dial Transplant. 2002; 17: 1157-59.
2.Sugerman HJ. Effects of increased intra-abdominal pressure in
severe obesity. Surg Clin North Am 2001; 81:1063-75.
3.Liese AD, Hense HW, Doring A, Stieber J, Keil U. Microalbuminuria,
central adiposity and hypertension in the non-diabetic urban population of
the MONICA Augsburg survey 1994/95. J Hum Hypertens 2001; 15:799-804.
4.Praga M, Hernandez E, Morales E et al. Clinical features and long-
term outcome of obesity-associated focal segmental glomerulosclerosis.
Nephrol Dial Transplant 2001; 9:1790-98.
5.Bonnet F, Deprele C, Sassolas A et al. Excessive body weight as a
new independent risk factor for clinical and pathological progression in
primary IgA nephritis. Am J Kidney Dis 2001; 37:720-27.
Competing interests:
None declared
Competing interests: No competing interests