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MO:
Growing up to double of the volume of glomerules Endotheliosis of glomerular cappilaries = marked tumefaction of endothelial cells with narrowed lumens and aspect of glomerules emptied of blood marked intersticial oedema with messangial hypercellularity extreme tummefaction of the glomerules may induce hernia of the glomerule in the initial TCP segment = onting
IF:
Subendothelial osmiofile deposits IgG, IgM and sometimes C deposits
Objective symptoms :
HTA over 145/90 mm Hg Oedematous syndrome Cardiomegalya, tachycardia with galloping rhythm Painfull hepatomegalya (due to stasis) Pallidness due to haemodilution
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Obstetrical complications :
abort Foetus death in uterus Retroplacental haematoma Hypotrophy or foetal prematurity
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Renal complications :
CRF during the last trimester of pregnancy
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Treatment
Prophylactic :
Hospitalization and investigations for the patients suspected of eclampsia Avoidance of diuretics (traditionally prescribed to every pregnant woman with oedema) Periodical check up of TA and G Periodical urine ex.
Curative
Objectives : - mothers protection against risks of HTA - maintenance of pregnancy as close as possible to the term day - assurance of a normal foetal development
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- Medicinal treatment
1 Anti-HTA treatment will be applied in cases of tension above 17/11 cmHg -Dopegyt, Aldomet 250-1000 mg/24 hrs -Hydrazinophtaleines 25-100 mg/24 hrs -Beta-blockers : Propranolol 40-120 mg/24 hrs, Atenolol 100-200 mg/24 hrs, Metoprolol 50-100 mg/24 hrs, Oxprenolol,Labetolol, etc -Clonidine 0,1-0,3 mg -Calcium antagonistics, but not before week 20 -Prozosin (Minipress) -Diazoxid 300 mg i.v., in case of great emergencie 2. Diuretic medication only in special situations (IC, EPA, eclampsia) 3. Antiadhezive aggregational medication and anticoagulant (controversial) Aspirin, Dipiridamole, Prostacycline, Heparyne, etc. 4. Sedative medication : barbiturates, benzodiazepines)
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SECONDARY NEPHROPATHY IN
PREGNANCY
2 Nephrotic syndrome
Appears in MCD, GNExM, GNMP, colagenousis, diabetic glomerulo- sclerosis, thrombosis of the renal veins, amyloidosis, syphilis, etc. Constitutes a group of high risk, necessitating a very special monitorise Risks : miscarrige, abortion, premature delivery, foetal hypotrophy, injury of maternal renal function Foetal supervision techniques : echography, tocography, hormonal mea-surements and checking up of amniotic liquid (relatioship lecytine with sphyngomyeline in the amniotic liquid)
SECONDARY NEPHROPATHY IN
PREGNANCY
4 HTA Chronic hypertension, irrespectively of the causes, i.e. reno-vascular HTA, co-arctation of aorta, Cushing disease, primary hyperaldosteronism, feo-chromocytome, etc. Maternal mortality amounts to 50 % in feochromocytom Chronic HTA with overadded pre-eclampsia (during the last trimestertakes the form of severe preeclampsia) Late or transitory HTA appears in multiparous women, who after carring succesive pregnancies, develop during the last part of pregnancy moderate HTA, recovering 10 days after delivery
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SECONDARY NEPHROPATHY IN
PREGNANCY
5 Pregnancy nephropathy in colagenousis
Lupus disease Pregnancy developes with apparently improvement of the nephropathy, but it exists a high frequency of foetal loses, predictible by dosing the Ac anti-cardio-lypine Occurance of pregnancy in LED must be strictly monitorised Maintenance of addapted doses of cortisone and imuran is recommanded, despite of the foetal risks Short treatment with corticoides high dosis immediatly after delivery Transplacental transfer of seric factor LE is possible PAN and SD cautious prognostication
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Worsening of renal function in 32 % of cases Raised TA in 38 % of cases Frequent appearance of overadded preeclampsia Further evolution of nephropathy after delivery in 13 % of cases Progressive worsening of renal function even after therapeutic abortion
8 Renal lithiasis
Raised frequency in pregnancy Usually there are phosphate calculies, secondary to infections In case of complications with risks of losing kidney, surgery is allowed even during pregnancy
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PREGNANCY
3 Bilaterale cortical necrosis Intervene in severe forms of acute renal failure, associating septicaemia and CIVD Possible mechanisms : coagulation necrosis in multiparous women with lesions of arteriolar diffuse sclerosis already present prolonged vaso-spasm with CIVD major clinic sign lake of reinstall of diuresis Certainty diagnosis = hystopathological (turgescent kidneys with glomerules entirely destroyed and capillaries obstructed by fybrinoid thrombis Irreversible evolution to uremia
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