**Laboratory diagnosis**

168 Basic Nephrology and Acute Kidney Injury

USG is usually diagnostic. Acute viral hepatitis in pregnancy presents as a systemic illness with fever, nausea, vomiting, fatigue, and jaundice, however, aminotransferase concentrations are markedly elevated (>500U/liter). The manifestations of pre-eclampsia are usually observed in the second half of pregnancy, whereas the symptoms of HELLP syndrome and AFLP frequently appear in the third trimester. The incidence of HELLP syndrome is much higher (1:5,000). Morbidity of the infant includes increased risk of cardiomyopathy, neuropathy, myopathy, nonketotic hypoglycemia, hepatic failure, and

 Functional hydronephrosis rarely cause renal failure. The diagnosis can be established in some cases by the normalization of renal function in the lateral recumbent position and its recurrence when supine. In some cases, either insertion of a ureteral catheter or delivery of the fetus is required. Rarely, acute urinary tract obstruction in pregnancy is induced by a

It refers to a syndrome characterized by arterial or venous thrombosis or specific pregnancy complications in women with laboratory evidence of antibodies to proteins bound to anionic phospholipids. International consensus conferences have proposed and revised classification criteria for definite APS ( Sapporo criteria)(Miyakis 2006). Definite APS is considered present if at least one of the following clinical criteria and at least one of the

1. Clinical —(a)Thrombosis — Unequivocal imaging or histologic evidence of thrombosis in any tissue or organ, OR (b) Pregnancy morbidity - Otherwise unexplained death at ≥10 weeks gestation of a morphologically normal fetus, OR One or more premature births before 34 weeks of gestation because of eclampsia, preeclampsia, or placental insufficiency, OR Three or more embryonic (<10 week gestation) pregnancy losses unexplained by maternal or paternal chromosomal abnormalities or maternal anatomic

2. Laboratory — The presence of antiphospholipid antibodies (aPL), on two or more occasions at least 12 weeks apart and no more than five years prior to clinical manifestations, as demonstrated by one or more of the following: (a)IgG and/or IgM aCL in moderate or high titer (>40 units GPL or MPL or > 99th percentile for the testing laboratory),(b)Antibodies to ß2-glycoprotein-I (ß2-GP-I) of IgG or IgM isotype at a titer >99th percentile for the testing laboratory when tested according to recommended procedures.(c)Lupus anticoagulant (LA) activity detected according to published

**Clinical manifestations** include deep vein thrombosis, thrombocytopenia, livedo reticularis, stroke, superficial thrombophlebitis, pulmonary embolism, fetal loss, transient ischemic attack, and hemolytic anemia. In rare patients, APS results in multiorgan failure because of multiple blood vessel occlusions, a condition referred to as "catastrophic antiphospholipid syndrome" In patients with preeclampsia or the HELLP syndrome, catastrophic APS must be considered, in patients with histories of thrombosis or spontaneous abortions . Thrombotic renal disease occurs in a minority of patients with APS. Glomerular capillaries and other renal vessels, both arteries and veins of all sizes, can be affected. The disease may

death associated with fatty acid oxidation defects in newborns.

**2.1.10 Urinary tract obstruction** 

**2.1.11 Antiphospholipid Syndrome (APS)** 

following laboratory criteria are satisfied.

or hormonal causes.

guidelines

kidney stone.

A history of a biologic false positive serologic test for syphilis (BFPTS) may be a clue to the presence of any type of aPL: aCL, ß2-GP-I antibodies, or an LA. However, because of the nonspecific nature of the BFPTS, the presence of one or more aPL should be confirmed with one of the tests (A)The presence of aPL may be demonstrated directly by: ELISA testing in the case of aCL and antibodies to ß2-GP-I and (B) Clotting assay that demonstrates effects of an aPL on the phospholipid-dependent factors in the coagulation cascade (LA test).The lupus anticoagulant phenomenon refers to the ability of aPL to cause prolongation of in vitro clotting assays such as the activated partial thromboplastin time (aPTT), the dilute Russell viper venom time (dRVVT), the kaolin clotting time or, the prothrombin time. This prolongation is not reversed when the patient's plasma is diluted 1:1 with normal plateletfree plasma.

**Treatment** includes heparin, oral anticoagulants ie warfarin, antiplatelet drugs eg aspirin and clopidogrel and hydroxyl chloroquin.
