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   Abstract
   Introduction
   Definition
   Classification
   Prevention of CKD
   Prevention of CK...
   Conclusion
   References
   Article Tables

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REVIEW ARTICLE
Year : 2007  |  Volume : 17  |  Issue : 2  |  Page : 47-52
 

Prevention of chronic kidney disease in children


Department of Nephrology and Chennai Pediatric Kidney Foundation, Mehta Children's Hospital, Chetpet, Chennai, Tamil Nadu, India

Correspondence Address:
M Vijayakumar
Flat 4, Muktha Vandan, Old No. 4, New No. 7, Ramanathan Street, Kilpauk, Chennai - 600 010, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-4065.37020

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  Abstract 

Chronic kidney disease (CKD) is being increasingly recognized in children, especially prevalent in those who recover from serious illness. The ability to recognize the pathophysiological conditions that predispose to renal parenchymal damage or disorders and the application of preventive measures or institution of ameliorating therapy may lessen the burden of the parenchymal damage leading to CKD. These measures include antenatal immunization, antenatal diagnosis, fetal surgical interventions and postnatal screening procedures for proteinuria, hypertension, dyslipidemia and prevention of obesity - all of which could play a significant role in the prevention of CKD or its progression to end stage renal disease.


Keywords: Antenatal prevention, children, chronic kidney disease, postnatal screening


How to cite this article:
Vijayakumar M, Nammalwar B R, Prahlad N. Prevention of chronic kidney disease in children. Indian J Nephrol 2007;17:47-52

How to cite this URL:
Vijayakumar M, Nammalwar B R, Prahlad N. Prevention of chronic kidney disease in children. Indian J Nephrol [serial online] 2007 [cited 2017 Mar 26];17:47-52. Available from: http://www.indianjnephrol.org/text.asp?2007/17/2/47/37020



  Introduction Top


Chronic kidney disease (CKD) is now being recognized worldwide as an important problem in children. The overt stage of CKD is the end stage renal disease (ESRD), which is merely the tip of the iceberg of a large number of "covert less severe diseases." CKD represents a developing process that is initiated by various causes, all with the common end result of persistent and usually progressive damage of varying severity to the kidneys. These patients have a continuous decline in renal function and hence are said to have progressive renal failure. It is characterized by the common histopathological end point of glomerulosclerosis, tubulointerstitial fibrosis and tubular atrophy, irrespective of the underlying etiology of kidney disease. The mechanisms involved in the progression of CKD are hemodynamic changes, hypertension and proteinuria, infiltration of inflammatory cells and local release of inflammatory cytokines and profibrogenic growth factors. The aim of this presentation is to identify the clinical and pathological conditions that cause renal damage and suggest measures for its prevention including screening procedures for the early detection of renal disease.


  Definition Top


A patient has CKD if either of the following criteria is present:

  1. Kidney damage for ≥3 months, as defined by structural or functional abnormalities of the kidney with or without decreased glomerular filtration rate (GFR) manifested by one or more of the following features:

    a. Abnormalities in the composition of the blood or urine

    b. Abnormalities in imaging tests

    c. Abnormalities on kidney biopsy


  2. GFR <60 ml/min/1.73 m 2 for ≥3 months with or without the other above-mentioned signs of kidney damages. [1]



  Classification Top


CKD has been classified into various stages for the purpose of prevention, early identification of renal damage and institution of preventive measures for progression of the primary damage and appropriate guidelines for instituting management for prevention of complications in severe CKD [Table - 1].


  Prevention of CKD Top


Pediatricians have the opportunity to screen at-risk patients, identify affected patients, prevent renal damage and ameliorate the impact of CKD by initiating early therapy and monitoring the disease progression. The prevention of CKD constitutes three important aspects.

Primary prevention aims to eliminate or reduce exposure to factors that cause renal disease. For CKD, this involves strategies to reduce antenatal exposure to infections, drugs and the prevention of inheritable renal disease by appropriate genetic counseling, prevention of obesity, dyslipidemia, early detection and appropriate management of hypertension and diabetes mellitus.

Secondary prevention in which the prevention of the progression of renal damage from stage 1 to stage 5 is carried out by introducing appropriate measures at various stages of CKD.

Tertiary prevention strategies are focus on the reduction or delay of long-term complications, impairments or disabilities in established disease, requiring renal replacement therapy (RRT).


  Prevention of CKD in Children Top


In adults, the primary causes of renal disease that progress into CKD are diabetes mellitus, atherosclerosis with or without hypertension and certain toxins. Hence, the primary preventive measures are limited to these few conditions. However, in children there is a wide range of conditions that can start even before birth; if not recognized earlier, these conditions can cause renal damage and progress to CKD in childhood, adolescence or later in the adult life. The preventive measures can be classified into antenatal and postnatal preventive measures.

Antenatal preventive measures

Intrauterine infections cause congenital nephrotic syndrome or malformation syndromes. Toxoplasmosis, congenital rubella and cytomegalovirus have been reported to cause renal damage. Antenatal preventive measures include appropriate antenatal immunizations to prevent rubella infection and appropriate screening and treatment of cytomegalovirus infection and toxoplasmosis.

Antenatal drugs such as ACE inhibitors (ACEI), angiotensin receptor blockers (ARB) or NSAIDs in early pregnancy can cause congenital anomalies. The histological examination of these children reveal tubular dysgenesis associated with poorly developed vasa recta. [2],[3],[4]

Familial clustering of ESRD in adults has been reported by several groups, including families with members having nephropathy associated with types 1 and 2 diabetes mellitus, hypertension, chronic glomerulonephritis, systemic lupus erythematosus and HIV infection. [5] In addition, a case control study by Lei et al., concluded that the familial clustering of kidney diseases occurred in excess of what could have occurred due to simple clustering of hypertension and diabetes mellitus within the families. [6] Children from such families have to be examined at frequent intervals for proteinuria, microalbuminuria and renal function, and the ultrasonogram of the abdomen is required, if indicated.

Genetic kidney disease (GKD) has been estimated to be the cause of 16% of ESRD, which increases up to 38% in an inbred community. [7],[8] Consanguinity is prevalent in some parts of India. Heredofamilial and congenital renal diseases are inherited in various patterns: X-linked, autosomal dominant or autosomal recessive. Some of the disorders appear to be caused by the defective synthesis or assembly of critical glycoproteins (collagen) components of the glomerular basement membrane and epithelial foot process. The following conditions with well-known genetic predisposition include Alport's syndrome, thin basement membrane nephropathy, Fabry's disease, lecithin-cholesterol acyltransferase deficiency, lipoprotein glomerulopathy, Finnish type of congenital nephrotic syndrome, diffuse mesangial sclerosis and familial focal segmental glomerulosclerosis, structural tubulointerstitial diseases such as polycystic kidney, nephronophthisis and medullary cystic diseases have a genetic predisposition. Metabolic tubulointerstitial diseases such as distal renal tubular acidosis, chronic hypokalemic disorders, hypercalciuric syndrome, Fanconi syndrome and hypophosphatemic rickets can lead to renal parenchymal damage and CKD. Congenital anomalies such as vesicoureteral reflux (VUR), posterior urethral valve (PUV) and mega-ureters have Mendelian inheritance. Atypical hemolytic uremic syndrome has a genetic basis.

Premarital genetic evaluation and counseling can probably play an important role in reducing such diseases. The study of family clustering, candidate gene case control association studies and genome screen analysis can help in identifying susceptible individuals and contribute in improving the clinical outcomes with far reaching implications for reducing CKD. [9] Gene therapy is on horizon. Until such high-tech feasibilities are available, simple prevention and correction of metabolic abnormalities can delay or prevent CKD. For example, the prevention of calcium deposition in hypercalciuric syndrome, Fanconi syndrome and renal tubular acidosis can go a long way in preventing interstitial damage and renal failure. Renal stone disease (RSD) is one of the causes of ESRD in adults. The commonest metabolic abnormality, namely, hypercalciuria and other urinary abnormalities often manifest from infancy and present in second or third decade of life as RSD. Early detection and appropriate preventive measures can reduce the burden of RSD in adults. Prevention of chronic hypokalemic states can prevent interstitial fibrosis and renal failure. Similarly, control of proteinuria in glomerular diseases can prevent renal damage. Antenatal ultrasonogram, amniotic fluid cytology, chorionic villus sampling and maternal serum alpha-fetoprotein estimation can detect early renal disorders and congenital anomalies. These findings can lead to possibility of fetal surgery or termination of pregnancy depending on the severity of abnormality and the likelihood of severe renal damage and irreversible renal failure.

Postnatal preventive measures

Congenital anomalies of kidney have been associated with CKD. Often the renal functions remain normal until growth (particularly at adolescent spurt) and increase in metabolic demands force a progressive decline in the renal function. ERSD develops by late childhood or adolescence. Dysplastic kidneys, PUV and VUR are a few of the well-known clinical disorders. [10],[11]

Renal hypoplasia represents a continuum ranging from renal agenesis to subtle congenital nephron deficits. The effect of Pax2 gene on apoptosis in the branching ureteric bud appears to imply a finely tuned quantitative process. Modest changes in this program could account for subtle nephron deficits in "normal" humans and confer an increased risk of hypertension or susceptibility to acquired renal diseases in later life. [12]

Renal agenesis : A high prevalence of proteinuria, glomerular sclerosis and renal failure have been documented in patients with unilateral renal agenesis. Experiments using the renal ablation model have established that a critical reduction in the number of functional nephrons leads to increase in the flow of glomerular plasma and capillary hydraulic pressure and glomerular hypertrophy in the remaining nephrons. These maladaptive hemodynamic and hypertrophic changes, together with an increase in the production of vasoactive and profibrogenic substances such as angiotensin II and endothelin and transforming growth factor β, contribute to structural and functional abnormalities, which if untreated lead to ESRD. It is possible that the coexistence of other urological malformations such as VUR, pelviureteric junction obstruction and ureterovesical junction obstruction can contribute to nephron loss in the patients with unilateral agenesis. It is observed that overweight plays a fundamental role in the appearance of proteinuria and renal damage in patients with severe renal mass reduction. [13]

Antenatal diagnosis of these congenital anomalies can facilitate appropriate postnatal evaluation. These tests include renal function tests, abdominal ultrasound, voiding cystourethrogram and the isotope evaluation for parenchymal structural abnormalities (dysplastic kidney) and obstructive disorders. These can determine preventive measures such as the correction of metabolic abnormalities, namely, polyuria, salt-losing states, hyperkalemia and bicarbonaturia. Early diagnosis can ensure the adequate drainage of urine with a clean intermittent catheterization (CIC) technique and surgical intervention in obstructive uropathy. These measures can prevent renal damage or the effects of the metabolic abnormalities on the functions of the kidney and its growth. Urodynamic studies can decide the need for drug therapy with or without CIC and prevent the damaging effects of retrograde pressure. The utility of ACEI and ARB for renoprotection in such situations has not been accepted universally. [14]

Birth weight is an important determinant of renal disease risk. In developing countries, low birth weight (LBW) babies are common in addition to the higher rates of superimposed intrauterine growth retardation (IUGR). The increasing retrieval of babies of very LBW associated with prematurity will produce a group with susceptibility to renal and related disorders in later life. Infants born with LBW have less number of nephrons predisposing to hypertension, cardiovascular events and altered renal function in adult life. The long-term renal consequences of LBW are generally attributed to the noxious effect of malnutrition on renal organogenesis resulting in a lower number of nephrons. Many of these children would have mild to moderate renal failure or hypertension. Adequate maternal nutrition, serial antenatal evaluation and therapeutic interventions can significantly reduce IUGR and LBW. Postnatal monitoring of these children for proteinuria, albuminuria and hypertension can detect early renal dysfunction and prevent the progression or delay the progress to grade 5 CKD or ESRD. Improved birth weight and better postnatal nutrition aiming only at moderate degree of overweight renders survival advantage in the same population. [15]

Obesity and the metabolic syndrome (Syndrome X) is on the rise among children and adolescents. [16] Obesity with a body mass index >27 kg/m 2 has been associated with microalbuminuria, proteinuria, poor renal function and histologically characterized by glomerulomegaly, mesangial expansion and/or sclerosis, which has been termed as "obesity related glomerulopathy". Obesity portends a poor prognosis in subjects with membranoproliferative GN (MPGN), IgA nephropathy and in those with single functioning kidney following nephrectomy. [17] If these individuals had hypertension, the incidence of microalbuminuria would be considerably higher. [18] The risk for glomerular hyperfiltration appears to be particularly high in those with abdominal obesity. Modest increases in the body fat act as risk multiplier factors in the presence of renal malformation, hypertension and diabetes. These factors are fueled in part by diets that are high in partially hydrogenated vegetable oils and low in fresh produce, consumption of carbonated drinks, [19] fast foods [20] as well as by an increase in the sedentary lifestyles as the children spend an average of 4-6 h/day watching television. Moreover, populations in which LBW and malnutrition are common may be predisposed to chronic kidney disease associated with weight gain, [21] and overweight or obesity are associated with increased congenital anomalies. Primary prevention will rely on controlling the global epidemic of obesity and associated type 2 diabetes as well as hypertension. Improved public health education on lifestyle modifications such as weight reduction, exercise and dietary manipulations can be effective. An approach to control hypertension by means of dietary salt restriction and diet rich in fruit and vegetables and low in saturated fat have been recommended. [22]

Infections : In developing countries, the high incidence of postinfectious glomerulonephritis, HIV/AIDS, hepatitis B, hepatitis C (rare in children) and other uncommon viral infections such as parvovirus, coronavirus, BK virus (in immunocompromised individuals), hepatitis A with hepato renal syndrome secondary to acute fulminant hepatitis, Epstein-Barr virus and dengue fever with multiorgan failure are the causes of acute kidney injury (AKI). [23] Parasitic infestations such as malaria, both falciparum and vivax, and schistosomiasis can cause renal damage. Incomplete recovery of renal damage from these illnesses can predispose to CKD in later life.

Metabolic diseases: In addition to the above-mentioned tubulointerstitial metabolic disorders, there are other systemic disorders that can predispose to systemic and renal vessel atherosclerosis and glomerulosclerosis. Diabetes mellitus, hyperlipidemic conditions and Syndrome X are few of them. Metabolic syndrome (Syndrome X) is defined as the clustering of obesity, dyslipidemia (high triglycerides and low high-density lipoproteins), elevated blood pressure, impaired glucose metabolism and insulin resistance. In recent times, the recognition of diabetes mellitus in children is on the rise. The impact of long-term type I diabetes on the renal function of these children has been recognized. Tight control of blood glucose with preventive measures against renal damage with ACEI or ARB or both will play a significant role in reducing the incidence of diabetic nephropathy.

Acute renal failure (ARF) or AKI results from complications of other systemic diseases including after heart surgery, neonatal care, bone marrow and solid organ transplantations. A study had shown 68% survivors with complete renal function and 13% with improved renal function. Sustained renal failure was observed in 12% survivors and 5% had progressed to ESRD. [24] As the risk for long-term renal injury is high, children should be periodically evaluated for signs of renal injury for years after the initiating event. In developing countries, the frequency of AKI following acute gastroenteritis and acute bacterial infections continue to be high in the list of etiologies. Natural calamities such as earth quakes and man-made disasters contribute a large population with trauma and crush injuries leading to AKI. The inevitable delay in management in such situations leads to residual renal damage and CKD. Appropriate education of health care professionals and public will assist in the initiation of early interventional therapies, namely, intravenous fluid administration at the site of accident, measures to prevent blood loss and hypovolemia, appropriate wound care and prevention of sepsis can reduce a large amount of AKI or its severity. Hemolytic uremic syndrome (HUS), particularly D-type, is associated with residual renal damage, hypertension and progression to CKD. [25] Early recognition and early intervention with dialysis or plasma infusion/exchange therapy is associated with good recovery.

Nephrotoxic drugs : Particularly drugs such as aminoglycosides, NSAIDs and contrast media should be used with great care, and combinations should be avoided wherever possible. Doses should be modified in the presence of renal insufficiency, hypovolemic and low cardiac output states. Even modified doses can be harmful in the presence of volume-depleted states, and particular care should be taken in ensuring good hydration before the administration of these drugs. Many patients are salt-losers in early stage, with poor ability to concentrate urine and are prone for hypovolemic states in the presence of trivial illness.

Screening procedures for early detection of renal disease

Primary hypertension among children is on an increase along with the epidemic of obesity. [26] In addition to causing CKD, hypertension can be the first indicator of CKD in children and adolescents. Patients with CKD and hypertension are at higher risk of loss of kidney function and development of cardiovascular diseases. Systemic hypertension causes direct damage to the small blood vessels in the nephron. The kidneys lose their ability to autoregulate glomerular filtration flow and pressure, with resultant hyperfiltration, manifesting as albuminuria. When the proximal convoluted tubule reabsorbs the excess protein, secretion of vasoactive substances further damages the glomerular-tubular apparatus. Nephron damage activates the renin-angiotensin-aldosterone system, resulting in an increased sympathetic tone and fluid overload, which compound the progression of hypertension and nephron loss. ACEI and ARB are more effective than other antihypertensive drugs in preventing the progression of kidney diseases. These agents lower intraglomerular pressure and proteinuria through their effect on systemic blood pressure as well as a direct action on glomerular circulation. The blockade of formation or action of angiotensin II exerts additional effects on fibrinolytic and/or inflammatory processes in the kidney. When ACEI therapy is initiated, some patients with CKD may have a mild increase in the serum creatinine and potassium levels. Therefore, serum creatinine and potassium levels should be monitored one to two weeks after the initiation of therapy and later at periodic intervals. Blood pressure measurement is mandatory in all children above 3 years of age during any medical examination and in children less than 3 years of age when admitted for serious renal or nonrenal diseases. The suggested doses of ACEIs and ARBs in children and infants are given in [Table - 2].

Proteinuria: Normal individuals usually excrete very small amounts of protein through the urine. Proteinuria is a marker of kidney injury, severity of CKD and a powerful independent predictor of its progression. Patients with persistently high rates of urinary protein excretion have a much faster rate of progression than those with mild or moderate proteinuria. [27] The excretion of specific types of protein, such as albumin or low molecular weight globulins, depends on the type of kidney disease. Increased excretion of albumin is a sensitive marker for CKD attributed to glomerular disease and hypertension. Loss of low molecular weight globulins in urine is a sensitive marker for tubulointerstitial disease. Patients with a positive dipstick test (1+ or greater) should undergo a quantitative measurement (protein-to-creatinine ratio) within 3 months. Patients with two or more positive quantitative tests temporally separated by 1-2 weeks can be labeled as having persistent proteinuria and warrant further examination for glomerular disease. While screening children for CKD, urine protein should be measured in a spot urine sample from the first morning urine specimen by either standard urine dipstick or by random protein-to-creatinine ratio. Urine protein concentrations can show significant diurnal variations. Most children who have proteinuria that does not persist on repeated testing may be considered to have transient proteinuria, a benign condition that is often associated with fever, stress or exercise.

Screening for proteinuria in the children in Japan represents an effective mass screening technique for the detection of asymptomatic glomerular disease and has been observed to prevent ESRD in children with MPGN and IgA nephropathies. [28] The American Academy of Pediatrics recommends that urine screening tests be conducted on two occasions during childhood: once before starting school and then again during adolescence. [29]

Microalbuminuria refers to albumin excretion above the normal range, but below the level of detection by dipstick for total protein. The test measures albumin, which is in very small quantities, hence the term microalbuminuria. It is a sensitive test for the early detection of parenchymal damage, particularly glomerular injury. In recent times, the determination of microalbuminuria has been indicated as an evidence for glomerular damage in many nondiabetic conditions such as polycystic kidney disease and chronic urinary tract infection. [30] There is a paucity of data. Microalbuminuria testing should be performed in children with normal GFR but with known renal parenchymal damage.

Dyslipidemia predisposes to diffuse atherosclerosis, and could lead to renal artery stenosis and renal ischemia and consequent renal dysfunction. The screening of children in families with familial dyslipidemia and institution of antilipidemic measures can prevent or delay atherosclerotic process. In addition, it is a risk factor for cardiovascular diseases progression of CKD. Most patients with CKD have an abnormal lipid panel that increases their risk for atherogenesis and hence the worsening of the kidney functions. The goals are the attainment of an LDL cholesterol level below 100 mg/dl and a triglyceride level below 200 mg/dl. Statins can safely and effectively lower the cholesterol levels. Atorvastatin is the recommended statin for use in children. Bile acid sequestrants appear to be safe and effective in improving dyslipidemias in children. Cholestyramine is the recommended bile sequestrant. The usual dosage of anhydrous cholestyramine is 80 mg/kg three times a day, not to exceed 8 g/day. Adverse effects are constipation, abdominal discomfort, nausea, flatulence, vomiting and anorexia. Bile acid sequestrant is generally mixed with 100-150 ml of water and increased fluid intake is recommended. Hence, this drug cannot be used in CKD patients who need to restrict fluids.


  Conclusion Top


A large number of clinicopathological conditions can produce renal damage in children. Anticipation, early recognition and institution of preventive measures can reduce the morbidity, mortality and the economic burden due to CKD. In a country like India, where dialysis and transplantation care is not within the reach of many children, steps should be taken to prevent the onset and progression of CKD in childhood.

 
  References Top

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2.Cooper WO, Hernandez-Diaz PH, Arbogast PG, Dudley JA, Dyer BS, Gideon PS, et al. Major congenital malformations after first-trimester exposure to ACE inhibitors. N Engl J Med 2006;354:2443-51.  Back to cited text no. 2    
3.Daikha-Dahmane F, Levy-Beff E, Jugie M, Lenclen R. Foetal kidney maldevelopment in maternal use of angiotension II type I receptor antagonists. Pediatr Nephrol 2006;21:729-32.  Back to cited text no. 3    
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29.Hogg RJ, Portman RJ, Milliner D, Lemley KV, Eddy A, Ingelfinger J. Evaluation and management of proteinuria and nephrotic syndrome in children: Recommendations from a pediatric nephrology panel established at the National Kidney Foundation Conference on Proteinuria, Albuminuria, Risk, Assessment, Detection and Elimination (PARADE). Pediatrics 2000;105:1242-9.  Back to cited text no. 29  [PUBMED]  [FULLTEXT]
30.Yudkin JS, Phillips DI, Stanner S. Proteinuria and progressive renal disease: Birth weight and microalbuminuria. Nephrol Dial Transplant 1997;12:10-3.  Back to cited text no. 30  [PUBMED]  



 
 
    Tables

  [Table - 1], [Table - 2]

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