Kidney In Systemic Diseases PDF

Kidney In Systemic Diseases Rasha Mahmoud Ass. Prof of Internal Medicine ¼ of patients with renal failure has hypertensive nephropathy Chr. hypertension damages the renal vasculature. Ischaernia and hyperfiltration cause nephrosclero...

Kidney In Systemic Diseases Rasha Mahmoud Ass. Prof of Internal Medicine ¼ of patients with renal failure has hypertensive nephropathy Chr. hypertension damages the renal vasculature. Ischaernia and hyperfiltration cause nephrosclerosis Hypertension is a risk of Cholesterol deposition , stenosis of renal arteries especially in patient more than 10 years history of hypertension The patient has hypertensive retinopathy.There is left ventricular hypertrophy on the ECG ,There is a long history of malignant hypertension.The proteinuria 100/µL or> 0.1 109/L (after a dwell time x of at least 2 hours), with> 50% polymorphonuclear; and c) positive dialysis effluent culture (lC). Management: gram-positive organisms be covered by vancomycin or a first generation cephalosporin and gram-negative organisms by a third-generation cephalosporin or an aminoglycoside (1B Acid Base disturbance Features of metabolic acidosis: Low plasma pH ~. Low plasma HCo3- concentration (;s1l_mmol/liter). Low arterial Co2 concentration (< 35 mmHg)..,....._,,--.,, Causes of elevated anion gap rnetabolic acidosis: MUDPILES Methanol, metabolism (inborn errors) Uremia Diabetic ketoacidosis Para ldehyde Iron, isoniazid Lactic acidosis Eth lene I col Salicylates, strychnine A. Renal causes: r>~45l- t!,4mrnon 1- Renal tubular acidosis (RTA): all l-;J/fS~ n,r~I &»,oh 80.P a. T I classic (Distal) RTA: inability to secrete H+ load. b. T e II proximal RTA: the PCT i unable to reab orb HCo3- RTA: There is both inability to secrete H+ load and proximal '--=-:;.__---' HCo3- wastage. d. T e IV RTA:This is u ually een in diabetic with mild renal impairment. 2- Diamox, a diuretic which causes bicarbonate wastage (bicarbonaturia). B-Gastrointestinalcauses I~ There i ~of~ and~-. 2- Fistula or tube drainage. 3- Ureterosigmoid or ileal loop urine diversion. 4- Anion exchange (CL- ver u HCo3-) a with the u e of ~styram~. ( it\ ~\,st-n.tc bve (f&ur\d,·ce) 5- Ingestion of Ca and Mg chlorides.  Clinical features Systemic effects of severe metabolic acidosis (oH ""'erect~t"att ot'\JdeP~ or..-e~P,v°'t,o"' ~ (Kussmaul's breathing, an increase in tidal volume, with deep, sighing respiration) and hyperventilation (to blow off CO2). J myocardial contractility, arteriodilatation, and venoconstriction · · ,...--) V,.tt\ hf CAA \ClY Resistant arrhythmias (esp. VF). r,\:>Yi\~bo\'\ The associated underlying cau e may be apparent. Metabolic alkalosis Metabolic alkalosis can only persist if there is a renal dysj a reduction in HCo3- excretion or enhanced renal generatio Features: High plasma HCo3- > 30 mmol/litre) High plasma pH (~ High Pco2 li~ > + are so us ow K+ is low as a rest r...__ ______ ______ __, '-)enteY~t ceU in_tr_a_c_e_ll_u_lar t.\tid ~e H~ P6K,,,te,,nr~. Causes A-Renal: 1- Adrenocorticoid and adrenocorticoid-like effect (HCo3- retention with K+ and H+ excretion): Secondary aldosteronism (e.g. cirrhosis) Prima aldosteronism Cushing's syndrome , Bartter's Liddle's and Gitelman's s ndromes d'f2- b Causes Severe respiratory disease e.g. obstructive air way disease and severe obesity. Central depression of respiratory drive. Clinical features: 1- Manifestations of the cause. 2- Confusion h erreactivit headache tremor stu or and coma in severe cases. 3- Papil1edema and increased CSF pre ure due to.D. -» ~u.'3e bYIA,·V\eJe)"V\Q,\ 4- Pulmonary and splanchnic IV.C.I Respiratory Alkalosis Excessive pulmonary wash of Co2 w: reduction in H+. The renal defense mechanism will inc ecretion and retention of H+. Thi met need 24 hour to be e tabli hed. Features: j pH >1 t-tS t PCo2 < ~s l HCo3 < i~ Causes: 0 1- Iatrogeni in patient under ventilatory support. ® 2- Liver cirr o i , alic I te int xicati n, exerci e and n 3- H er~ntilation ndrome in ne otic patient. 4- Cerel:>al hypoxia and intracrania di ea e Clinical features : 1- Manife of the cau e 2- Paresth~si~. tinnitu , neuromu cular irritability and/or cerebral vasocon tnction  Nephrotic Syndrome - It is a clinical syndrome characterized by : 1- Heavy proteinuria ( more than 3.5 gm/24 hours in adults). 2- H ypoproteinaemia. 3- Generalized oedema. 4 - Hyperlipidaemia. - The primary abnormality in nephrotic syndrome is the heavy proteinuria with other manifestations occurring secondary to it Aetiology: I. Primary glomerulonephritis: Minimal lesion GN ( the most common cause in children ) Membranous GN ( the most common cause in adults). Membranoproliterative GN. Focal segmental glomerulosclerosis. II. Secondary (3Is + 3Ms) a) Immune diseases : SLE (systemic lupus), PAN (polyarteritis nodosa) & anaphylactoid purpura ,Serum sickness ,Mixed cryoglobulinaemia. b) Infections : Hepat~tis C ~ B ,HIV nephroP.athy ,Infective endocarditis ,Syphilis Ma1ana, Sch1stosoma manson1. Clinical Picture : 1. Nephrotic oedema - It is of gradual onset. - It begins in the periorbital region, face then involves 2. Pallor: due to oedema & anaemia. 3. Gastrointestinal manifestations: : anorexia, nausea, vomiting & diarrhoea due to oedema of gastric & intestinal mucosa. 4. Parotid enlargement, white nails (leuconychia), muscle wasting & osteoporosis: may be present due to hypoproteinaemia. 5. Features of the cause: e.g. DM, SLE. 6) rfemporarr impairment of renal functions :- May occasionally end in acute kidney injury in severe cases. Pathogene i : - in·ury of glomeruli. --------- - thrombo i of glomerular capillarie. - acute tubular necro i due to glomerular i cha m1a. - tubular ob truction by ca t. Nephritic Syn.dro e Definition Diseases characterized by acute onset : 4- Oedema. 1- Oliguria 5-Azotemia 2- Haematuria. 3- Hyperten ion. 6-Protienuria. Aetiology I. lr_yGN: Proliferative - membrano-proliferative GN. II. 2ry GN: (4 Is) : 1) Infection : , Bacterial: Group-A fl.i haemolytic streptococci (most common) in acute Lon illitis & in pyoderma. , Viral: HBV, CMV, EBY. , Parasitic: Schi to oma, pla modium. 2) Iatrogenic: e.g. Penicillin. 3) Immunological di ease : e.g. SLE, Rhumatoid, PAN. 4) Others:- Irradiation - Kidney rejection. Injury of glomerili -+Haematuria. Pathological changes:  Clinical Picture : 1) Haematuria: Usually in the form of dark or smoky urine but fra Pathogenesis : injury of the capillary wall. 2) Oliguria : due to decreased glomerular pern 3) Nephritic oedema : Of acute onset. 4) Cardiovascular manifestations a) Hypertension : - It is due to salt & water retention. - Severe hypertension may lead to HF , pulmonary oedema hemorrhage. b) Circulatory congestion: - Congested pulsating neck veins & pulmonary congestion - Due to hypervolaemia or uncommonly heart failure. 5) General manifestations - Fever, headache & malaise. - Anorexia, nausea & vomiting. - Pain in both loins. - Pallor due to oedema & anaemia Glomerular diseases Clinical presentation Asymptomatic (much common) Severe disease Hypertension AKI Proteinuria Severe extra-renal disease haematuria during routine medical work Clinical presentation of various glomerular disease Asymptomatic Macroscopichematuria Nephrotic syndrome Proteinuria: adult >3.5 g/day; Brown/red painless hematuria Proteinuria 150 mg to 3 g per day child >40 mg/h per m2 (no clots); typically coincides with Hematuria >2 red blood cells Hypoalbuminemia 10 x 106 cells/liter Hypercholesterolemia between attacks (red blood cells usually dysmorphic) Lipiduria Nephritic syndrome RPGN Chronicglomerulonephritis Oliguria Renal failure over days/weeks Hypertension Hematuria: red cell casts Proteinuria usually< 3 g/day Renal impairment Proteinuria: usually 3 g/day Edema Blood pressure often normal Shrunken smooth kidneys Hypertension May have other features of vascullt,s