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Pathology -Chronic renal disease.
Definition: A progressive and irreversible loss in renal function, classified into five phases based on estimated glomerular filtration rate (eGFR) (Table 9.1).
Epidemiology: Diabetes and kidney vascular disease contribute to the high prevalence of this condition. Aetiology • Diabetic and hypertensive nephropathy are the leading causes. • Other causes include reflex nephropathy, obstructive nephropathy, IgA nephropathy (IgAN), focal segmental glomerulosclerosis (FSGS), membranous nephropathy, systemic lupus erythematosus (SLE), myeloma, amyloidosis, medications, gout, and adult polycystic kidney disease (APKD).
Pathogenesis • A decrease in nephron mass below a certain level can lead to progressive renal damage, regardless of the underlying disease. • The sequence of events causing progressive renal damage is thought to be glomerular hyperfiltration, hypertension, injury, glomerulosclerosis, and tubulointerstitial fibrosis. • TGF-B plays a vital role in promoting renal scarring. Early illness is asymptomatic and can only be detected by measuring eGFR in at-risk patients, such as diabetics or hypertensives. • As patients advance, they become weary and have bone pain.
• End-stage renal failure patients with fluid overload and metabolic abnormalities may require prompt renal replacement therapy. Biochemistry • Urea and creatinine levels are elevated due to poor waste product excretion. • Reduced Calcium due to a shortage of active calcitriol. • increase Phosphate due to inadequate phosphate excretion. • Secondary hyperparathyroidism caused by low calcium levels. •Reduced haemoglobin levels due to decreased erythropoietin production.Loss of acid-base and sodium/potassium equilibrium happens later in chronic renal disease.
Complications • High risk of cardiovascular disease due to hypertension, vascular calcification, and hyperlipidemia. • Deranged calcium and phosphate metabolism causes renal bone disease, a complicated combination of hyperparathyroidism, osteomalacia, and osteoporosis.
Definition: A progressive and irreversible loss in renal function, classified into five phases based on estimated glomerular filtration rate (eGFR) (Table 9.1).
Epidemiology: Diabetes and kidney vascular disease contribute to the high prevalence of this condition. Aetiology • Diabetic and hypertensive nephropathy are the leading causes. • Other causes include reflex nephropathy, obstructive nephropathy, IgA nephropathy (IgAN), focal segmental glomerulosclerosis (FSGS), membranous nephropathy, systemic lupus erythematosus (SLE), myeloma, amyloidosis, medications, gout, and adult polycystic kidney disease (APKD).
Pathogenesis • A decrease in nephron mass below a certain level can lead to progressive renal damage, regardless of the underlying disease. • The sequence of events causing progressive renal damage is thought to be glomerular hyperfiltration, hypertension, injury, glomerulosclerosis, and tubulointerstitial fibrosis. • TGF-B plays a vital role in promoting renal scarring. Early illness is asymptomatic and can only be detected by measuring eGFR in at-risk patients, such as diabetics or hypertensives. • As patients advance, they become weary and have bone pain.
• End-stage renal failure patients with fluid overload and metabolic abnormalities may require prompt renal replacement therapy. Biochemistry • Urea and creatinine levels are elevated due to poor waste product excretion. • Reduced Calcium due to a shortage of active calcitriol. • increase Phosphate due to inadequate phosphate excretion. • Secondary hyperparathyroidism caused by low calcium levels. •Reduced haemoglobin levels due to decreased erythropoietin production.Loss of acid-base and sodium/potassium equilibrium happens later in chronic renal disease.
Complications • High risk of cardiovascular disease due to hypertension, vascular calcification, and hyperlipidemia. • Deranged calcium and phosphate metabolism causes renal bone disease, a complicated combination of hyperparathyroidism, osteomalacia, and osteoporosis.
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