Kidney diseases 2024.pptx

Kidney diseases Overview of kidney diseases Nephritis Nephrotic syndrome Renal failure Learning outcomes  To know the common symptoms and signs of renal tract diseases  To understand pathogenesis of nephritis, nephrotic syndrome and renal failure  To describe the main clinical characteristics...

Kidney diseases Overview of kidney diseases Nephritis Nephrotic syndrome Renal failure Learning outcomes  To know the common symptoms and signs of renal tract diseases  To understand pathogenesis of nephritis, nephrotic syndrome and renal failure  To describe the main clinical characteristics of these diseases Kidney diseases Overview of kidney diseases Nephritis Nephrotic syndrome Renal failure Clinical overview Kidney’s principal function − Eliminating waste materials − Regulating fluid & electrolyte balance as well as acid-base balance − Endocrine function (prostaglandins, erythropoietin, 1,25-(OH)2-D3, renin) Most diseases of kidney are associated with abnormalities of the glomerular capillary or the renal tubule system Sensitive to various immune reactions − immune complexes deposited in the glomerular capillary walls The symptoms suggesting renal tract disease: − − − − − Dysuria Haematuria Urinary retention Alteration of urine volume (either polyuria or oliguria) Pain situated along the renal tract Diseases of Kidney Glomeruli – immunologically mediated Tubules – toxic/infectious agents Interstitium – toxic/infectious agents Blood vessels –  blood supply damage Severe damage to all four structures  Chronic renal diseases  Renal failure Kidney diseases Overview of kidney diseases Nephritis Nephrotic syndrome Renal failure Nephritis Inflammation of any part of the kidney 1. Glomerulonephritis (GN) 2. Interstitial nephritis 3. Pyelonephritis Glomerulonephritis A general term for a group of disorders: − bilateral, symmetrical immunologically mediated injury to the glomerulus Accounts for 1/3 cases of terminal renal failure Primary – kidney is the predominant organ involved (e.g. post-streptococcal glomerulonephritis) Secondary – systemic diseases with glomerular involvement (e.g. SLE) Glomerulonephritis In situ formation of immune complex Deposition of circulating Immune complex Deposition of anti-GBM Cell-mediated glomerular damage Inflammatory response Secondary mechanisms Hypercellularity Basement membrane thickening Hyalinisation and sclerosis Acute nephritic syndrome Nephrotic syndrome Renal failure, acute & chronic Asymptomatic proteinuria Microscopic haematuria Exogenous antigen e.g. Infective agents (Group A  -haemolytic Strep.) Endogenous antigen e.g. SLE Acute nephritic syndrome Acute nephritic syndrome Pathology: Diffuse proliferative glomerulonephritis - hypercellular glomeruli Management: Supportive measures until spontaneous recovery Hypertension: salt restriction, diuretics, vasodilators Fluid balance monitoring In oliguric with fluid overload, fluid restriction Management of life-threatening complications Clinical featrures: Haematuria Proteinuria Hypertension Oedema (periorbital) Oliguria & uraemia Moderate impairment of renal function & reversible Normal glomerulus Acute proliferative glomerulonephritis Kidney diseases Overview of kidney diseases Nephritis Nephrotic syndrome Renal failure Certain glomerular diseases Other primary & secondary GN Nephrotic syndrome GBM damage loss of electrostatic & physical barriers Characterised by severe proteinuria & generally lead to chronic kidney dysfunction  synthesis of lipid protein in liver + abnormal transport of circulating lipid  catabolism Hyperlipidaemia Nephrotic syndrome passage of large MW proteins into the glomerular filtrate Proteinuria  Protein loss +  catabolism of protein in the kidney Hypoalbuminaemia ↓Plasma oncotic pressure hypovolemia ↑renin-angiotension-aldosterone ↑Na and water retention Oedema Normal glomerulus Membranous nephropathy Certain glomerular diseases Other primary & secondary GN Nephrotic syndrome GBM damage loss of electrostatic & physical barriers Diagnostic investigation passage of large MW proteins into the glomerular filtrate Proteinuria (>3.5g/24 h in adults)  Protein loss +  catabolism of protein in the kidney  synthesis of lipid protein in liver + abnormal transport of circulating lipid  catabolism Hyperlipidaemia Hypoalbuminaemia (serum albumin 40mmol/L: − Oliguria, oedema − Plasma creatinine rises (by ~ 100 mol/day) − Hyperkalaemia & metabolic acidosis − Uraemic syndrome: anorexia, nausea, vomiting, irritability, seizures, coma Acute renal failure ─ Treatment Correct reversible underlying factors eg. volume depletion, nephrotoxic drugs  Treat hyperkalaemia  Dialysis - Indications: Hyperkalaemia (> 6.5 mmol/L ) Severe metabolic acidosis (pH 40mmol/L − Uraemic syndrome:  Nervous system (malaise, loss of energy, loss of appetite, insomnia)  Gastrointestinal (nausea, vomiting, and diarrhea)  Dermatological (itching) – Nocturia and polyuria – Oedema Chronic renal failure ─ Haematological and metabolic complications Anaemia − − − − Largely due to EPO deficiency Normochromic, normocytic Typical “anaemia of chronic disease” Responds to EPO Renal osteodystrophy Electrolyte/acid-base disorders − − Hyperkalaemia; Na retention (usually) Hypo~ (early) & hyper~ (late) -calcaemia − Metabolic acidosis Which of the following kidney structure is most prone to immunological damage? (a) Glomeruli (b) Renal tubules (c) Interstitium (d) Blood vessels (e) None of the above Chronic renal failure is most commonly caused by: (a) Kidney stones (b) Hypertension (c) Streptococcal infection (d) Renal blood vessel defect (e) All of the above