REGIONAL SCIENTIFIC WORKSHOP OF THE NIGERIAN ASSOCIATION OF NEPHROLOGY

HEART DISEASE AND CHRONIC KIDNEY DISEASE IN CHILDREN. BY PROF OLOWU A.O. PAEDIATRICS DEPT. OOUTH
The Chairman Prof. G.B. Ogunmola Resident, Nigerian Association of Nephrology Chairman, NAN ducation Committee Chairman, !OC meritus Professor and "oyen of Nigerian Nephrology Prof. A#in#ug$e O.O. Other eminent Nephrologists, Cardiologist and %cholars "istinguished !adies and Gentlemen. INTRODUCTION: &t 'as 'ith great pleasure that & accepted the in(itation from the !OC of this NAN regional scientific workshop to present a paper on the su$)ect The Heart in Chronic Kidney Diseases in Children. The heart and the #idney are t'o (ery (ital organs in the human $eing. The heart is $asically responsi$le for pumping enough $lood to meet the meta$olic re*uirements of the $ody, 'hile the #idney help to maintain the internal mile (ia its e+cretory and secretary functions. ,alfunctioning of either organ could affect the functions of the other. The focus of this presentation is its highlight the effect of Chronic Renal Diseases (CRD) on the heart in children. DEFINITION: A chronic #idney disease is a renal damage 'ith or 'ithout decreased Glomer lar !ilteration Rate (G!R), manifested as pathological a$normalities or mar#ers of #idney damage and a G-R . /ml0min0/.12,3 PREVALENCE: The pre(alence of CR" is $elie(ed to $e on the increase, though no national figures are a(aila$le. &n %agamu 4OO5T67, CR" accounted for 8.9: of all paediatric admissions o(er a t'o;year period 4388< 38897

AETIOLOGY OF PAEDIATRIC CRD

Causes of CR" in childhood include= 4a7 Congenital ,alformations of >idneys and 5rinary tract. 4$7 Renal hypoplasia ? dysplasia Bilateral se(ere (esico;ureteral reflu+ Posterior urethral (al(e These usually manifest 'ith signs of chronic renal failure $efore 9 years. Glomerular "isorders ,em$rano Proliferature glomerulonephritis -ocal and segmented glomerulosclerosis 4@uartan ,alaria Nephropathy7 Glomerulonephropathy in systemic diseases e.g. systemic !upus rythematosus Chronic Pyelonephritis

4c7 6ereditary Renal "iseases Polycystic renal disease Alport syndrome Nephronophthisis Congenital nephrotic syndrome Renal lesion of !a'rence ,oon Biedl %yndrome &n CR", the end;stage is chronic renal failure 4CR-7 'hich manifests 'ith progressi(ely decrease G-R. >idneys ha(e great capacity to adapt to an e+tensi(e reduction in the num$er of functioning nephrons e.g. G-R may $e reduced to a$out 39: $efore clinical signs of renal failure appear. %ummary
G-R Plasma P8<2 Ca3? plasma Parathyroid 6ormone %ecretion Tu$ular AAAAAAAAAAAAAAAAA Rea$sorption of P8<2 Tu$ular rea$sorption of Ca3?

PATHOPHYSIOLOGY

B%erum Ca3?
CCa3? rea$sorption from gut due to relati(e Ditamin " resistance

END RESULT Gro'th arrest and retardation 6ypocalcemia, 6yperphosphatemia 6yperparathyroid $one disease 4renal osteodystrophy7 Normocytic, normochronic anaemia ,eta$olic acidosis 5raemia, 6yper#alaemia 6ypertension

THE HEART IN CKD There is paucity of literature on the cardiac in(ol(ement in CR" among paediatric age group. Ee #no' that the heart could $e affected in children 'ith CR"s. %ome possi$le mechanisms for this include anaemia, hypertension, uraemia and hyper#alamia. Chronic n !"i : A decreased erythropoiesis is 'ell documented in patients 'ith CR". %uggested mechanisms F Cerythropoietin production $y the #idneys CTG of RBC Blood !oss "efecti(e utiliHation of &ron and folate 6aemodynamic changes to anaemia Cardiac output at rest and after e+ercise is increased in chronic anaemia especially 'hen the haemoglo$in le(el is less than 1gm0dl. This is due to increased stro#e (olume, since tachycardia is fre*uently not found. The afterload has $een found to decrease 'hile myocardial contractility is increased. Plasma (olume is slightly increased, 'hile total $lood (olume and central $lood (olume 4CBD7 are decreased. The latter ho'e(er is usually increased in anaemic congesti(e state. Blood transformation may decrease CBD in some patients and increase in others. This response cannot $e predicted from the initial le(el of right atrial pressure 4RAP7. &t is therefore

ad(isa$le to correct anaemia in patients 'ith CR" (ery slo'ly, 'ith the use of pac#ed cells rather than 'hole $lood and to monitor RAP during the transfusion. H#$!r%!n&ion: This is defined as a consistent $lood pressure measurement I J9th

percentile for age and se+. 6ypertension in childhood is fre*uently secondary to renal pathology. A *uarter 439:7 of our patients 'ith chronic renal failure in %agamu had moderate to se(ere hypertension, though figures from other centers (ary from 28: to 98:. %uggested mechanisms for renal hypertension &ncreased rennin secretion from the " #ta Glomer lar $pparat s ("G$) &ncreased peripheral (ascular resistance in uraemic patients &ncreased plasma concentration of endothelin an endothelium deri(ed (asoconstricti(e peptide in uremia Treatment 'ith human erythropoietin Clinical effects of sustained hypertension Cardiomegaly, left (entricular hypertrophy ? strain ,yocardial dysfunction Congesti(e cardiac failure 4c7 Ur !"i : 5raemia may cause myocardial dysfunction )ust li#e sustained meta$olic acidosis. Other cardiac effects include= Pericarditis manifested as friction ru$s in the left parasternal area. Pericardial effusion usually mild to moderate 4d7 H#$!r' ( !"i : 6yper#alaemia reduces the ratio of the >? concentration inside the cell to that outside it, there$y depolariHing the myocardium. This 'ill result in decreased conduction (elocity and increased rate of repolariHation. The le(el of > ? in the serum can $e predicted from the electrocardiogram $ecause of the different effects on the action potential. %erum >? . 9.9m. *0!

,ild hyper#alaemia. &t may actually ser(e as an anti;arrhythmic $ecause it reduces the automaticity of ectopic pace;ma#ers and terminate re;entrant arrhythmias.

%erum >? I 9.9 K.9m. *0! CG e(idence Tall, tented T 'a(es

This is moderate hyper#alaemia This is ho'e(er a poor sign of hyper#alaemia many normal children ha(e it, 'hile some children 'ith B serum >? do not ha(e it. %erum > I K.K;1.8 m *0! This is se(ere hyper#alaemia CG e(idence B PR &nter(al, 'idening of @R% comple+, BBB pattern %erum >? I 1.8 m *0!

&nter;atrial conduction delay L -lattening of P 'a(es %erum >? I M.9 m *0! (ery se(ere hyper#alaemia CG e(idence Atrio(entricular )unctional escape rhythm, 'ith a$sence of P 'a(es A sine 'a(e pattern produced $y the merging of 'idened @R% comple+ 'ith T 'a(e Dentricular tachycardia and (entricular fi$rillation The electrophysiological effects of hyper#alaemia are potentiated $y hyponatremia, hypocalcemia and hypomagnesemia $ecause these decrease the mem$rane threshold potential. 6ence they can result in cardioto+icity at lo'er than e+pected >? concentration.

CONCLUSION
The heart is in(aria$ly affected in children 'ith CR" through the effects of anaemia, hypertension, uremia, meta$olic acidosis and hyper#alemia. There is need for a (ery cautious approach to management of a child 'ith CR" especially in deciding 'hether or not to transfuse. &n depth studies of the state of the heart in children 'ith CR" in this en(ironment is suggested.

REFERENCES
/. ,a$ayo)e ,.O. Chronic >idney "isease. Nephrology Association of Nigeria Conference !ecture 3. !oge N.P., !ange R." and ,oore C.D. CharacteriHation of the anaemia association 'ith chronic renal insufficiency. Am. N. med /J9M=3<=<;/M 2. Naco$son !.O., Gold'asser ., -ried E. and PiHa# !. Role of the #idney in erythropoiesis. Nature /J91F /1J=K22;< <. RemuHHi G. and Rossi .C. 6aematological conse*uences of renal failure= &n Brenner B.,., !e(ine %.A. 4eds7. The >idney E.B. %aunders Company Philadelphia, !ondon, Toronto, ,ontreal, %ydney, To#yo /JJK page 3/18;MK 9. Daral ,.A., Adolph R.N. and -o'ler N.O. cardio(ascular effects of anaemia. A.,. 6eart N. /J13FM2427=</9;3K K. 6offin !. . Primary T 'a(e changes in children. Pra+is /J19=K<=M82;//