Chronic Kidney disease Year 4 Paediatrics Notes OmpathStudy

Chronic Kidney disease Year 4 · Paediatrics Collection: 4TH YEAR ALL NOTES / PAEDS / PAEDS 4.2 / MUNGE / RENAL PAEDS -- Slide 1 Chronic Kidney Disease Dr Rose Munge Slide 2 Introduction Chronic kidney disease (CKD) is determined by the presence of kidney damage and level (or severity) of kidney function (glomerular filtration rate, or GFR.\n End-stage renal disease (ESRD) is an administrative term in the United States; it is used to define all patients who are treated with dialysis or kidney transplantation, and is a subset of patients with stage 5 CKD. Slide 3 Patient has chronic kidney disease (CKD) if either of the following criteria are present: 1. Kidney damage for ≥ 3 mo, as defined by structural or functional abnormalities of the kidney, with or without decreased GFR, manifested by one or more of the following features:\n• Abnormalities in the composition of the blood or urine\n• Abnormalities in imaging tests\n• Abnormalities on kidney biopsy 2. GFR < 60 mL/min/1.73 m2 for ≥ 3 mo, with or without the other signs of kidney damage described above Slide 4 STAGE DESCRIPTION GFR (mL/min/1.73 m2 ) 1 Kidney damage with normal or increased GFR ≥90 2 Kidney damage with mild decrease in GFR 60-89 3 Moderate decrease in GFR 30-59 4 Severe decrease in GFR 15-29 5 Kidney failure <15 or on dialysis Slide 5 The pediatric CKD prevalence is approximately 18 per 1 million children.\nThe prognosis for the infant, child, or adolescent with CKD has improved dramatically since the 1970s, mostly because of improved medical management, dialysis techniques, and kidney transplantation.\nYet, childhood-onset ESRD still carries significant morbidity and a 30-fold increased mortality rate as compared with healthy peers, with cardiovascular and infectious diseases as the leading causes of death. Slide 6 The etiology of pediatric CKD may be the result of congenital, acquired, inherited, or metabolic renal disease; causes of kidney disease in children are typically subdivided as being either nonglomerular or glomerular in origin.\nThe underlying cause correlates with the age at the time of diagnosis. In children < 5 yr of age, CKD is most commonly a result of congenital abnormalities of the kidney and urinary tract (i.e., renal hypoplasia, dysplasia, or obstructive uropathy) and is often diagnosed with prenatal ultrasonography.\nIn children older than 5 yr of age, acquired or inherited forms of glomerulonephritis predominate. Slide 8 In addition to progressive injury with ongoing structural or metabolic genetic diseases, renal injury can progress despite removal of the original insult. Hyperfiltration injury may be an important final common pathway of glomerular destruction, independent of the underlying cause of renal injury.\nAs nephrons are lost, the remaining nephrons undergo structural and functional hypertrophy characterized by an increase in glomerular blood flow.\nThe driving force for glomerular filtration is thereby increased in the surviving nephrons. Although this compensatory hyperfiltration temporarily preserves total renal function, it can cause progressive damage to the surviving glomeruli, possibly by a direct effect of the elevated hydrostatic pressure on the integrity of the capillary wall and/or the toxic effect of increased protein traffic across the capillary wall.\nOver time, the remaining nephrons suffer an increased excretory burden, resulting in a vicious cycle of increasing glomerular blood flow and hyperfiltration injury. Slide 9 Other pathologic etiologies of chronic kidney disease include proteinuria, hypertension, hyperphosphatemia, and hyperlipidemia.\nProteinuria itself can contribute to renal functional decline.\nProteins that traverse the glomerular capillary wall can exert a direct toxic effect on tubular cells and recruit monocytes and macrophages, enhancing the process of glomerular sclerosis and tubulointerstitial fibrosis.\nUncontrolled hypertension can exacerbate the disease progression by causing arteriolar nephrosclerosis and by increasing the hyperfiltration injury. Hyperphosphatemia can increase the progression of disease by leading to calcium phosphate deposition in the renal interstitium and blood vessels.\nHyperlipidemia, a common condition in CKD patients, can adversely affect glomerular function through oxidant-mediated injury.\nCKD is viewed as a continuum of disease, with increasing biochemical and clinical manifestations as renal function deteriorates. Regardless of the etiology, the progression of tubulointerstitial fibrosis is the primary determinant of CKD progression. Slide 10 Clinical Manifestations The clinical presentation of CKD is varied and depends on the underlying etiology and CKD stage.\nCAKUT and some genetic forms of renal disease (i.e., familial nephronophthisis) demonstrate growth failure, vomiting, and polyuria with associated polydipsia.\nUrinary tract infection can also be common in those with urologic abnormalities. Glomerular forms of CKD often present with