{"id":2800,"date":"2015-04-28T06:25:51","date_gmt":"2015-04-28T06:25:51","guid":{"rendered":"http:\/\/biomedpharmajournal.org\/?p=2800"},"modified":"2016-10-05T10:59:10","modified_gmt":"2016-10-05T10:59:10","slug":"evaluation-of-biochemical-markers-and-oxidative-stress-in-females-of-acute-renal-failure","status":"publish","type":"post","link":"https:\/\/biomedpharmajournal.org\/staging\/vol6no2\/evaluation-of-biochemical-markers-and-oxidative-stress-in-females-of-acute-renal-failure\/","title":{"rendered":"Evaluation of Biochemical Markers and Oxidative Stress in Females of Acute Renal Failure"},"content":{"rendered":"

Introduction<\/strong><\/p>\n

Over the last three decades, several experimental models have identified pathophysiologic mechanisms associated with acute renal failure and have enhanced our understanding of the disease.(1, 2, 3)<\/sup> Acute renal failure result from alteration in renal perfusion, changes in glomerular filtration, and tubular dysfunction and \u00a0correction of these factors can ameliorate the effects of acute renal failure.(4)<\/sup> Acute renal failure usually occurs as the results of a sudden interruption in the blood supply to the kidney or \u00a0toxic overload of the kidney.(5)<\/sup> Oxidative stress has been reported with increasing age.(6)<\/sup> Reactive oxygen species are important mediators of injury in acute renal failure. Under normal physiologic conditions, a homeostatic balance exists between the formation of reactive oxygen species and their removal by endogenous antioxidant compounds.(7)<\/sup> A major lesson from all of these studies reveals that acute renal failure is frequently reversible.(8)<\/sup><\/p>\n

Materials and Mathods<\/strong><\/p>\n

The clinical material for present study comprised 58 female patients of acute renal failure admitted in G. M. and S. G. M. Hospital, S. S. Medical College, Rewa (M. P.), India. 60 healthy female subjects of same age group were selected as control. The age range was taken from 30 to 80 years. Blood samples were collected from the patients at the time of admission as well as from individuals of female healthy control groups. Clinical investigations were performed in the Department of Biochemistry, S. S.\u00a0 Medical College, Rewa (M. P.), India. Serum protein (Total), creatinine, urea, and superoxide dismutase were estimated by biuret, jaffe\u2019s, diacetyl monoxime, and Mishra H P et al methods respectively. Plasma malondialdehyde and haemolysate glutathione reductase, glutathione peroxidase, and catalase, were estimated by Jean C D et al method (1983), Horn H D (1963), Hafeman D G method (1974), and Asror K sinha method (1972) respectively. Serum electrolytes were estimated by electrolyte analyzer. Obtained data were analyzed statistically by using student \u201ct\u201d test.<\/p>\n

Observations<\/strong><\/p>\n

Table 1: Comparative study of biochemical parameters between female healthy control and female acute renal failure group (age 30 \u2013 50 years).\u00a0 <\/strong><\/p>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
S. No.<\/strong><\/td>\nParticulars<\/strong><\/td>\nFemale healthy control\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 <\/strong><\/p>\n

(30)<\/strong><\/td>\n

Female acute renal failure (30)<\/strong><\/td>\nt-test<\/strong><\/td>\nP-value<\/strong><\/td>\n<\/tr>\n
Mean<\/strong> \u00b1 S. D.<\/strong><\/td>\nMean<\/strong> \u00b1 S. D.<\/strong><\/td>\n<\/tr>\n
1<\/strong><\/td>\nSerum Sodium ions (mEq \/ L)<\/td>\n139.99 \u00b1 2.46<\/td>\n127.07 \u00b1 3.05<\/td>\n18.060<\/td>\n< 0.001<\/td>\n<\/tr>\n
2<\/strong><\/td>\nSerum Potassium ions (mEq \/ L)<\/td>\n4.42 \u00b1 0.32<\/td>\n6.13 \u00b1 0.28<\/td>\n22.027<\/td>\n< 0.001<\/td>\n<\/tr>\n
3<\/strong><\/td>\nSerum Glucose (mg \/ dl)<\/td>\n87.61 \u00b1 4.63<\/td>\n119.87 \u00b1 3.84<\/td>\n29.375<\/td>\n< 0.001<\/td>\n<\/tr>\n
4<\/strong><\/td>\nSerum Protein (Total) (gm \/ dl)<\/td>\n7.19 \u00b1 0.17<\/td>\n6.14 \u00b1 0.21<\/td>\n21.286<\/td>\n< 0.001<\/td>\n<\/tr>\n
5<\/strong><\/td>\nSerum Creatinine (mg \/ dl)<\/td>\n0.8 \u00b1 0.11<\/td>\n3.05 \u00b1 0.35<\/td>\n33.591<\/td>\n< 0.001<\/td>\n<\/tr>\n
6<\/strong><\/td>\nSerum Urea (mg \/ dl)<\/td>\n29.82 \u00b1 1.85<\/td>\n44.97 \u00b1 1.30<\/td>\n36.699<\/td>\n< 0.001<\/td>\n<\/tr>\n
7<\/strong><\/td>\nS-Superoxide dismutase (EU \/ mg protein \/ ml)<\/td>\n13.06 \u00b1 1.34<\/td>\n9.50 \u00b1 0.29<\/td>\n14.222<\/td>\n< 0.001<\/td>\n<\/tr>\n
8<\/strong><\/td>\nGlutathione reductase (EU \/ gm protein)<\/td>\n19.65 \u00b1 0.16<\/td>\n17.99 \u00b1 0.06<\/td>\n53.208<\/td>\n< 0.001<\/td>\n<\/tr>\n
9<\/strong><\/td>\nGlutathione peroxidase (EU \/ mg % Hb)<\/td>\n9.62 \u00b1 0.28<\/td>\n7.52 \u00b1 0.08<\/td>\n39.499<\/td>\n< 0.001<\/td>\n<\/tr>\n
10<\/strong><\/td>\nCatalase (EU \/ mg protein \/ ml)<\/td>\n6.09 \u00b1 0.19<\/td>\n4.79 \u00b1 0.06<\/td>\n35.736<\/td>\n< 0.001<\/td>\n<\/tr>\n
11<\/strong><\/td>\nPlasma Malondialdehyde (nano mole \/ ml)<\/td>\n3.97 \u00b1 0.77<\/td>\n9.55 \u00b1 0.28<\/td>\n37.302<\/td>\n< 0.001<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

\u00a0<\/strong><\/p>\n

Table 2: Comparative study of biochemical parameters between female healthy control and female acute renal failure group (age 51 \u2013 80 years). <\/strong><\/p>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
S. No.<\/strong><\/td>\nParticulars<\/strong><\/td>\nFemale healthy control\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 <\/strong><\/p>\n

(30)<\/strong><\/td>\n

Female acute renal failure (28)<\/strong><\/td>\nt-test<\/strong><\/td>\nP-value<\/strong><\/td>\n<\/tr>\n
Mean<\/strong> \u00b1 S. D.<\/strong><\/td>\nMean<\/strong> \u00b1 S. D.<\/strong><\/td>\n<\/tr>\n
1<\/strong><\/td>\nSerum Sodium ions (mEq \/ L)<\/td>\n141.36 \u00b1 2.97<\/td>\n123.07 \u00b1 3.24<\/td>\n22.431<\/td>\n< 0.001<\/td>\n<\/tr>\n
2<\/strong><\/td>\nSerum Potassium ions (mEq \/ L)<\/td>\n5.08 \u00b1 0.32<\/td>\n6.73 \u00b1 0.39<\/td>\n17.664<\/td>\n< 0.001<\/td>\n<\/tr>\n
3<\/strong><\/td>\nSerum Glucose (mg \/ dl)<\/td>\n99.48 \u00b1 2.96<\/td>\n121.36 \u00b1 3.53<\/td>\n25.604<\/td>\n< 0.001<\/td>\n<\/tr>\n
4<\/strong><\/td>\nSerum Protein (gm \/ dl)<\/td>\n7.47 \u00b1 0.29<\/td>\n6.09 \u00b1 0.23<\/td>\n19.985<\/td>\n< 0.001<\/td>\n<\/tr>\n
5<\/strong><\/td>\nSerum Creatinine (mg \/ dl)<\/td>\n0.89 \u00b1 0.09<\/td>\n3.28 \u00b1 0.34<\/td>\n37.154<\/td>\n< 0.001<\/td>\n<\/tr>\n
6<\/strong><\/td>\nSerum Urea (mg \/ dl)<\/td>\n35.52 \u00b1 2.77<\/td>\n48.89 \u00b1 2.51<\/td>\n19.216<\/td>\n< 0.001<\/td>\n<\/tr>\n
7<\/strong><\/td>\nS-Superoxide dismutase (EU \/ mg protein \/ ml)<\/td>\n12.41 \u00b1 1.61<\/td>\n8.93 \u00b1 0.45<\/td>\n11.036<\/td>\n< 0.001<\/td>\n<\/tr>\n
8<\/strong><\/td>\nGlutathione reductase (EU \/ gm protein)<\/td>\n18.79 \u00b1 0.27<\/td>\n17.71 \u00b1 0.05<\/td>\n20.824<\/td>\n< 0.001<\/td>\n<\/tr>\n
9<\/strong><\/td>\nGlutathione peroxidase (EU \/ mg % Hb)<\/td>\n8.9 \u00b1 0.15<\/td>\n6.99 \u00b1 0.06<\/td>\n62.822<\/td>\n< 0.001<\/td>\n<\/tr>\n
10<\/strong><\/td>\nCatalase (EU \/ mg protein \/ ml)<\/td>\n5.39 \u00b1 0.17<\/td>\n4.33 \u00b10.09<\/td>\n29.365<\/td>\n< 0.001<\/td>\n<\/tr>\n
11<\/strong><\/td>\nPlasma Malondialdehyde (nano mole \/ ml)<\/td>\n3.35 \u00b1 0.36<\/td>\n9.91 \u00b1 0.25<\/td>\n80.055<\/td>\n< 0.001<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

\u00a0<\/strong><\/p>\n

Table 3: Comparative study of biochemical parameters between 30 \u2013 50 and 51 \u2013 80 years age group of female acute renal failure patients. \u00a0<\/strong><\/p>\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n\n
S. No.<\/strong><\/td>\nParticulars<\/strong><\/td>\nFemale acute renal failure <\/strong><\/td>\nt-test<\/strong><\/td>\nP-value<\/strong><\/td>\n<\/tr>\n
(30\u201350Yr<\/sup>) Mean<\/strong> \u00b1 S. D. (30)<\/strong><\/td>\n(51\u201380Yr<\/sup>) Mean<\/strong> \u00b1 S. D. (28)<\/strong><\/td>\n<\/tr>\n
1<\/strong><\/td>\nSerum Sodium ions (mEq \/ L)<\/td>\n127.07 \u00b1 3.05<\/td>\n123.07 \u00b1 3.24<\/td>\n4.843<\/td>\n< 0.001<\/td>\n<\/tr>\n
2<\/strong><\/td>\nSerum Potassium ions (mEq \/ L)<\/td>\n6.13 \u00b1 0.28<\/td>\n6.73 \u00b1 0.39<\/td>\n6.765<\/td>\n< 0.001<\/td>\n<\/tr>\n
3<\/strong><\/td>\nSerum Glucose (mg \/ dl)<\/td>\n119.87 \u00b1 3.84<\/td>\n121.36 \u00b1 3.53<\/td>\n1.535<\/td>\n0.130<\/td>\n<\/tr>\n
4<\/strong><\/td>\nSerum Protein (Total) (gm \/ dl)<\/td>\n6.14 \u00b1 0.21<\/td>\n6.09 \u00b1 0.23<\/td>\n0.865<\/td>\n0.390<\/td>\n<\/tr>\n
5<\/strong><\/td>\nSerum Creatinine (mg \/ dl)<\/td>\n3.05 \u00b1 0.35<\/td>\n3.28 \u00b1 0.34<\/td>\n2.536<\/td>\n< 0.05<\/td>\n<\/tr>\n
6<\/strong><\/td>\nSerum Urea (mg \/ dl)<\/td>\n44.97 \u00b1 1.30<\/td>\n48.89 \u00b1 2.51<\/td>\n7.542<\/td>\n< 0.001<\/td>\n<\/tr>\n
7<\/strong><\/td>\nS-Superoxide dismutase (EU \/ mg protein \/ ml)<\/td>\n9.50 \u00b1 0.29<\/td>\n8.93 \u00b1 0.45<\/td>\n5.773<\/td>\n< 0.001<\/td>\n<\/tr>\n
8<\/strong><\/td>\nGlutathione reductase (EU \/ gm protein)<\/td>\n17.99 \u00b1 0.06<\/td>\n17.71 \u00b1 0.05<\/td>\n19.233<\/td>\n< 0.001<\/td>\n<\/tr>\n
9<\/strong><\/td>\nGlutathione peroxidase (EU \/ mg % Hb)<\/td>\n7.52 \u00b1 0.08<\/td>\n6.99 \u00b1 0.06<\/td>\n28.383<\/td>\n< 0.001<\/td>\n<\/tr>\n
10<\/strong><\/td>\nCatalase (EU \/ mg protein \/ ml)<\/td>\n4.79 \u00b1 0.06<\/td>\n4.33 \u00b1 0.09<\/td>\n23.047<\/td>\n< 0.001<\/td>\n<\/tr>\n
11<\/strong><\/td>\nPlasma Malondialdehyde (nano mole \/ ml)<\/td>\n9.55 \u00b1 0.28<\/td>\n9.91 \u00b1 0.25<\/td>\n5.151<\/td>\n< 0.001<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

\u00a0<\/strong><\/p>\n

Results<\/strong><\/p>\n

We observed, highly significant (p<0.001) increased biochemical values in serum potassium ions, glucose, creatinine, urea and plasma malondialdehyde when compared to female healthy control groups (Table: 1 and 2).<\/p>\n

Biochemical markers such as serum sodium ions, protein (Total),\u00a0 superoxide dismutase, and haemolysate glutathione reductase, glutathione peroxidase and catalase were decreased showing highly significant (p<0.001) in female acute renal failure when compared to control groups (Table: 1 and 2).<\/p>\n

Comparative study of acute renal failure between age 30 \u2013 50 and 51 \u2013 80 years shows\u00a0 levels of sodium ions, superoxide dismutase, glutathione reductase, glutathione peroxidase, and catalase were decreased, highly significant (p<0.001) in age 51 \u2013 80 years of acute renal failure when compared to acute renal failure age 30 \u2013 50 years. Highly significant (p<0.001) increased levels of potassium ions, urea and plasma malondialdehyde were observed in age 51 \u2013 80 years of females suffering from acute renal failure. Serum creatinine was increased significantly (< 0.05) in acute renal failure between age 51 \u2013 80 years.<\/p>\n

Discussion and Conclusion<\/strong><\/p>\n

Acute renal failure is usually considered a disease of the hospitalized patients. Although this is often true, acute renal failure may occur in the outpatients setting.(8)<\/sup> Acute renal failure in the hospital setting is often iatrogenic, a result of medical intervention. Incidence of acute renal failure in hospitalized patients is between 2 to 5 per cent.(9)<\/sup> Advance age, liver diseases, underlying renal insufficiency and diabetes (especially in the presence of vascular disease) have been implicated as risk factor for the development of acute renal failure.(8)<\/sup> Acute tubular necrosis is the most common cause of intrinsic acute renal failure in hospitalized patients. Ischemia or toxins usually induce this condition.\u00a0 Ischemic acute tubular necrosis is frequently reversible, but if the ischemia is severe enough to cause cortical necrosis, irreversible renal failure can occur.(10, 11)<\/sup> Acute tubular necrosis may be prevented by promptly treating patients with reversible causes of ischemic or pre-renal acute renal failure and by maintaining appropriate hydration in patients who are receiving nephrotoxins.(12)<\/sup><\/p>\n

Acute renal failure, the kidneys are unable to perform their normal excretory function leading to accumulation of renally eliminated electrolytes.(13)<\/sup> Hyponatremia is a relatively common complication of acute renal failure due to a dilution effect by retained water.(14)<\/sup> Euvolemic hyponatremia<\/em> t<\/em>he most common type of hyponatremia seen in hospitalized acute renal failure patients.(15, 16, 17)<\/sup> A 38.6 per cent incidence of hyperkalemia is seen in azotemic patients.(18)<\/sup> Acute renal failure is potential complication of hyperkalemia, affects potassium excretion due to reduced nephron mass (number of functioning collecting ducts) and intrinsic impairment of active potassium secretion(19)<\/sup>, because the number of collecting ducts is directly related to the glomerular filtration rate, renal failure whether acute or chronic, leads to impaired renal potassium secretion.(20)<\/sup> Pathophysiology of hyperglycemia is associated with hyponatremia in advanced renal failure. Hyperglycemia causes disturbances in the tonicity of body fluids, the distribution of body water between major body fluid compartments and the external balance of body solute and water.(21)<\/sup> The prevalence of proteinuria was three times as great among those individuals with a self-reported family history of kidney disease and proteinuria is directly reduces serum protein levels.(22)<\/sup> Elevated serum creatinine levels are common in the community and \u00a0strongly associated with older age.(23) <\/sup>Nitrogenous waste products from protein metabolism are retained in the body, resulting in azotemia, as evidenced by the increased serum levels of urea nitrogen.(24)<\/sup> \u00a0Similar results were observed in our study (Table: 1 and 2).<\/p>\n

Oxygen is required by various systems for the release of energy and to detoxify xenobiotics. The products of partial reduction of oxygen are referred to as \u2018reactive oxygen species\u2019 which are highly reactive.(25)<\/sup> Generation of reactive oxygen species contribute to oxidative and the renal damage in ischemic- acute renal failure (iARF).(26)<\/sup> Oxidative stress was measured by reduced level enzymatic activity of superoxide dismutase and catalase.(27) <\/sup>Oxygen free radical scavengers protect against ischemia \/ reperfusion injury of the kidney in vivo and against hypoxia \/ re-oxygenation (H \/ R) injury of renal cells in several in vitro systems acute injury.(28) <\/sup>Oxygen free radicals have been implicated in the pathogenesis of ischaemic acute renal failure. Plasma glutathione peroxidase levels were significantly lower in the patients with post diarrhoeal acute renal failure.(29) <\/sup>Malondialdehyde is a terminal product of lipid peroxidation, which can be measured in plasma and serves as an effective lipid peroxidation marker and an indirect index of reactive oxygen species activity.(30)<\/sup> Acute renal failure can be triggered or aggravated by reactive oxygen species but established ARF per se might also affect the antioxidant defense mechanisms of the organism.\u00a0 In patients with associated ARF was even more pronounced and plasma malondialdehyde levels were higher.(27, 31)<\/sup> Similar results were observed in our study (Table: 1 and 2).<\/p>\n

Acute renal failure is most commonly seen in older adults and its associated with significant mortality and morbidity, with death rates among hospitalized acute renal failure patients ranging from 25 to 70 per cent.(32, 33)<\/sup> Acute renal failure is characterized by tubular dysfunction with impaired sodium and water re absorption and it has associated with the shedding and excretion of proximal tubule brush border membranes and epithelial tubular cells into the urine.(11)<\/sup> An evolving understanding of epidemiology and patho physiology of acute organ dysfunction in the setting of critical illness has give rise to new concepts and terminology for a syndrome once known as either acute tubular necrosis or acute renal failure.(34)<\/sup><\/p>\n

Hyperkalemia could be caused by an overall excess of body potassium or by a shift from inside to outside cells or hyperkalemia could be caused by the sudden release of potassium ions from muscle into the surrounding fluids.(35, 36)<\/sup> With acute renal failure, sustained decline in the glomerular filtration rate, which leads to accumulation of nitrogenous waste products and uremic toxin.(37)<\/sup> Acute renal failure can be triggered or aggravated by reactive oxygen species but established acute renal failure per se might also affects the antioxidant defense mechanisms of the organism.(38)<\/sup> Superoxide dismutase is generally thought to play a central role because it scavenges superoxide anion at the initial step of the radical chain reaction.(39)<\/sup><\/p>\n

Therefore, from above study we are concluding that acute renal failure are associated with increased serum potassium (hyperkalemia), creatinine, urea and plasma malondialdehyde and decreased serum sodium (hyponatremia), antioxidant enzymes are also associated with the disease. The main novel finding of this study is that oxidative stress leads to acute renal failure. Oxidative stress in elderly patients intensified especially if the patients have associated with renal complications especially in middle age.<\/p>\n

References<\/strong><\/p>\n

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