Postpartum Renal Failure Research Articles

Applying the WHO ICD-MM classification system to maternal deaths in a tertiary hospital in Nigeria: A retrospective analysis from 2014-2018.

BackgroundAddressing the problem of maternal mortality in Nigeria requires proper identification of maternal deaths and their underlying causes in order to focus evidence-based interventions to decrease mortality and avert morbidity.ObjectivesThe objective of the study was to classify maternal deaths that occurred at a Nigerian teaching hospital using the WHO International Classification of Diseases Maternal mortality (ICD-MM) tool.MethodsThis was a retrospective observational study of all maternal deaths that occurred in a tertiary Nigerian hospital from 1st January 2014 to 31st December,2018. The WHO ICD-MM classification system for maternal deaths was used to classify the type, group, and specific underlying cause of identified maternal deaths. Descriptive analysis was performed using Statistical Package for Social Sciences (SPSS). Categorical and continuous variables were summarized respectively as proportions and means (standard deviations).ResultsThe institutional maternal mortality ratio was 831/100,000 live births. Maternal deaths occurred mainly amongst women aged 25–34 years;30(57.7%), without formal education; 22(42.3%), married;47(90.4%), unbooked;24(46.2%) and have delivered at least twice;34(65.4%). The leading causes of maternal death were hypertensive disorders in pregnancy, childbirth, and the puerperium (36.5%), obstetric haemorrhage (30.8%), and pregnancy related infections (17.3%). Application of the WHO ICD-MM resulted in reclassification of underlying cause for 3.8% of maternal deaths. Postpartum renal failure (25.0%), postpartum coagulation defects (17.3%) and puerperal sepsis (15.4%) were the leading final causes of death. Among maternal deaths, type 1, 2, and 3 delays were seen in 30(66.7%), 22(48.9%), and 6(13.3%), respectively.ConclusionOur institutional maternal mortality ratio remains high. Hypertensive disorders during pregnancy, childbirth, and the puerperium and obstetric haemorrhage are the leading causes of maternal deaths. Implementation of evidence-based interventions both at the hospital and community levels may help in tackling the identified underlying causes of maternal mortality in Nigeria.

Post-partum acute renal failure: A case report

Post-partum acute renal failure: A case report

Demographics and Outcomes Associated With End Stage Renal Disease After Pregnancy Related Acute Kidney Injury [3E

INTRODUCTION: Pregnancy related acute kidney injury (AKI) remains an important cause of maternal and fetal morbidity and mortality, which can result in end-stage renal disease (ESRD) requiring life-long renal replacement. Little is known about the characteristics of those who develop ESRD after pregnancy related AKI. METHODS: The United States Renal Data System (USRDS) national registry between 1990 and 2015 was used to analyze the frequency of postpartum renal failure and associated risk factors. We used Cox proportional hazards models to evaluate risk factors for mortality and access to transplant among those with post-partum ESRD. RESULTS: There were 224 cases of ESRD due to post-partum renal failure vs 151,974 reproductive age women who developed ESRD secondary to other causes. Minorities were disproportionately affected: African-American women comprised 28.6% of those with post-partum renal failure but only represented 15.7% of births over the same time period. Similarly, Hispanic women represented 28.0% of those with post-partum renal failure but only 20% of live births. African-Americans with ESRD due to post-partum renal failure had a 2.15-fold higher hazard of mortality. Women with post-partum renal failure had better overall survival compared other causes of renal failure (HR=0.38, p<0.001). Despite this, women with post-partum renal failure had 0.45 lower hazards of receiving a kidney transplant, even after adjusting for demographic characteristics (P<.001). CONCLUSION: There are racial disparities in development of post-partum ESRD, with African-American and Hispanic women disproportionately affected. Women with post-partum ESRD are significantly less likely to receive a transplant despite having better overall survival.

119. The management of pregnant women with chronic kidney disease: An 8-year review in a tertiary care center

Objective The management and treatment of kidney disease has advanced, and women who are pregnant and give birth have also increased recently. On the other hand, pregnancy with kidney disease causes preeclampsia (19–30%), intrauterine fetal death (16–20%), postpartum renal failure (3–5%). The purpose of this study was to review the maternal and neonatal outcomes in pregnant women with chronic kidney disease (CKD), and to evaluate the appropriate management that may contribute to obstetric outcomes. Methods We conducted a retrospective review of 126 births and 129 neonates in 110 CKD patients who were seen at Osaka University Hospital between January, 2010, and December, 2017. Results The mean patient age was 33.5 (18–49) years, and the nulliparity rate was 61%. The most frequent disease was IgA nephropathy (43/126; 34%) and the second was lupus nephritis and renal transplantation (both were 15/126; 12%). Second trimester abortion and preterm delivery occurred in 5% and 20% of the patients, respectively. There was no maternal and neonatal death. Fetal growth restriction and preeclampsia occurred in 10% and 25% of the patients, respectively. Two patients with lupus nephritis and one with Henoch-Schonlein purpura nephritis had severe preeclampsia occurred before 20 weeks gestation. sFlt1/PlGF ratio were 427, 865 and 1183, respectively. Conclusions To predict and prevent the adverse events in the care of pregnant women with CKD is important for good maternal and neonatal outcomes. Furthermore, Henoch-Schonlein purpura nephritis that had been already ameliorated may be also a risk factor for severe preeclampsia.

Pregnancy: Kidney Diseases and Hypertension

Pregnancy: Kidney Diseases and Hypertension

Postpartum autoimmune thyroid syndrome.

Postpartum thyroid dysfunction is rather a common problem during postpartum period, found in approximately 5% of mothers in the general population. It occurs from subclinical autoimmune thyroiditis that is aggravated after parturition and causes various types of thyroid dysfunction. Immune activity is physiologically suppressed during pregnancy so that the fetus is not rejected, and rebounds above the normal level after parturition. Graves' disease and Hashimoto's thyroiditis spontaneously ameliorate during pregnancy, and are often aggravated after parturition. The high-risk mothers for postpartum thyroid dysfunction can be well screened by anti-thyroid microsomal antibody (MCAb) and 60% to 70% of MCAb-positive mothers develop postpartum thyroid dysfunction, which is transient in most cases. New onset of Graves' disease may be screened by thyroid stimulating antibody (TSAb) and 70% of TSAb-positive mothers develop either transient or persistent postpartum Graves' disease that usually occurs at 3-6 months postpartum. Immune rebound after parturition may not cause only autoimmune thyroid diseases but other autoimmune Table 4. Various types of postpartum autoimmune disease diseases, which may be investigated with the similar strategies to those in postpartum autoimmune thyroid disease. Thus, we found that postpartum onset of rheumatoid arthritis occured in 0.08% of women in the general population and could be partially predicted by measuring rheumatoid factors in early pregnancy. There are several case reports of other autoimmune diseases developed after delivery; postpartum renal failure or post-delivery hemolyticuremic syndrome, postpartum idiopathic polymyositls, postpartum syndrome with antiphospholipid antibodies, postpartum autoimmune myocarditis. Many other possible postpartum autoimmune diseases are still unexplored. Postpartum autoimmune thyroid syndrome is a good model for understanding the mechanism of onset and aggravation of other autoimmune diseases. Prediction and prevention of postpartum onset of many autoimmune diseases could be established in the near future.

Postpartum autoimmune thyroid syndrome: a model of aggravation of autoimmune disease.

Postpartum thyroid dysfunction is rather a common problem during the postpartum period being found in approximately 5% of mothers in the general population. It occurs from subclinical autoimmune thyroiditis that is aggravated after parturition and causes various types of thyroid dysfunction. Immune activity is physiologically suppressed during pregnancy so that the fetus is not rejected, and rebounds above the normal level after parturition. Graves' disease and Hashimoto's thyroiditis also spontaneously ameliorate during pregnancy, and are often aggravated after parturition. The high-risk mothers for postpartum thyroid dysfunction are well screened by antithyroid microsomal antibody (MCAb) and 60% to 70% of MCAb-positive mothers develop postpartum thyroid dysfunction, which is transient in most cases. New onset of Graves' disease may be screened by thyroid-stimulating antibody (TSAb) and 70% of TSAb-positive mothers develop either transient or persistent postpartum Graves' disease that usually occurs 3 to 6 months postpartum. Immune rebound after parturition may cause not only autoimmune thyroid diseases but other autoimmune diseases, which may be investigated with similar strategies to those in postpartum autoimmune thyroid disease. Thus, we found that postpartum onset of rheumatoid arthritis was found in 0.08% of women in the general population and could be partially predicted by measuring rheumatoid factors in early pregnancy. There are several case reports of other autoimmune diseases that develop after delivery; postpartum renal failure or postdelivery hemolytic-uremic syndrome, postpartum idiopathic polymyositis, postpartum syndrome with antiphospholipid antibodies, postpartum autoimmune myocarditis. Many other possible postpartum autoimmune diseases are still unexplored. Puerperal diseases should be carefully examined in relation to autoimmune abnormalities in the affected organs.

Postpartum renal failure: a complex case with probable coexistence of hemolysis, elevated liver enzymes, low platelet count, and hemolytic uremic syndrome

Background: Postpartum renal failure in previously healthy subjects is associated most often with preeclampsia and/or hypertension; hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome, hemolytic uremic syndrome; or thrombotic thrombocytopenic purpura. Transient oliguria associated with preeclampsia is common, but renal failure is rare. Coexistence of HELLP and hemolytic uremic syndromes has been suggested, but histopathologic documentation of this combination has been scarce. Case: A 30-year-old primigravida with severe preeclampsia at 35 weeks and 3 days’ gestation presented with the development of HELLP syndrome and renal failure postpartum. Histopathologic lesions characteristic of hemolytic uremic syndrome were present in the kidney. Conclusion: Probable overlapping of HELLP and hemolytic uremic syndromes in pregnancy or postpartum should be taken into consideration when treating patients with these syndromes and associated complications, such as renal failure.

Acute Renal Failure in Pregnancy

From 1976 to 1994, 57 women were referred to the Centro de Nefrología, Montevideo, with obstetric acute renal failure (ARF). The main causes were hypertensive disorders such as preeclampsia (PE) in 27, acute pyelonephritis of pregnancy (APN) in 26, and idiopathic postpartum renal failure in 3. Severe preeclampsia superimposed on chronic hypertension and acute pyelonephritis of pregnancy complicated by sepsis accounted for more than 50% of the cases of ARF. Chronic renal failure developed in 6 patients: 2 had bilateral renal cortical necrosis, 1 had malignant nephrosclerosis, and 3 had idiopathic postpartum renal failure. Maternal mortality related to ARF was low in this group of patients (less than 2%). In contrast, perinatal mortality was strikingly high (40%).

6 Acute renal failure in pregnancy

Acute renal failure (ARF) has become a very rare complication of pregnancy. This results from the virtual disappearance of septic abortion ARF and from the improvement of prenatal care, including the prevention of volume contraction which is mainly due to uterine haemorrhage, early diagnosis, and treatment of other classic maternal complications such as pre-eclampsia and acute pyelonephritis. The incidence of bilateral renal cortical necrosis has also been declining during the last decade. Acute fatty liver, a potentially fatal disease, is often complicated by ARF. Early recognition of this disorder, with prompt termination of pregnancy and intensive supportive therapy, can reduce fetal and maternal mortality rate. The syndrome of idiopathic postpartum renal failure is also associated with a high morbidity and mortality. Beyond supportive treatment, including haemodialysis or peritoneal dialysis and the use of potent antihypertensive drugs to control blood pressure and blood transfusion if necessary, specific therapy as plasma infusion, plasma exchange and antiplatelet drugs may be of value. Both peritoneal dialysis and haemodialysis may be used in gravidas with ARF. Early 'prophylactic' dialysis should be applied to pregnant women. Careful monitoring of fluid balance and anticoagulation is necessary during dialysis.

Postpartum eclampsia and acute renal failure; treatment with prostacyclin. Case report

Postpartum eclampsia and acute renal failure; treatment with prostacyclin. Case report

Lupus Anticoagulant Associated with Renal Thrombotic Microangiopathy and Pregnancy-Related Renal Failure

The clinical features in 12 women with a circulating coagulation inhibitor (lupus 'anticoagulant') were studied and correlated with findings in 22 renal biopsies in these patients. Four of 12 women had serological evidence of systemic lupus. Only two of 23 pregnancies in these women were successful. Lesions in all biopsies were remarkably similar. Seven biopsies taken during or soon after pregnancy showed acute fibrinoid lesions. 'Acute' lesions consisted of fibrin thrombi in glomeruli arterioles and arteries and double contours in glomerular capillary walls. Biopsies carried out remote from pregnancy in these seven patients showed persisting double contours in glomeruli together with narrowing of arteries due to recanalizing thrombi and cellular intimal proliferation. All other biopsies showed similar lesions. The lesions were essentially the same as those of thrombotic microangiopathy and those described previously in post-partum renal failure. Renal function was severely impaired in four patients and showed moderate impairment in two patients at the time that acute thrombotic lesions were demonstrated in glomeruli. Renal function in two patients improved during plasma exchange therapy. Because all biopsies showed either acute, healing or healed, thrombotic lesions, it is proposed that these lesions are characteristic of the renal findings in patients with a lupus 'anticoagulant'. In all but two cases the acute lesions were seen during or soon after pregnancy.

6 Acute renal failure in pregnancy

Acute renal failure has become a very rare complication of pregnancy. This results from the virtual disappearance of septic abortion ARF and from the improvement of prenatal care, including the prevention of volume contraction which is mainly due to uterine haemorrhage, early diagnosis, and treatment of other classic maternal complications such as pre-eclampsia and acute pyelonephritis. The incidence of BRCN has also been declining during the last decade. Acute fatty liver, a potentially fatal disease, is often complicated by ARF. Early recognition of this disorder with prompt termination of pregnancy and intensive supportive therapy can reduce fetal and maternal mortality rate. The syndrome of idiopathic postpartum renal failure is also associated with a high morbidity and mortality. Beyond supportive treatment including haemo- or peritoneal dialysis, the use of potent antihypertensive drugs to control blood pressure and blood transfusion if necessary, specific therapy as plasma infusion, plasma exchange and antiplatelet drugs may be of value. Both peritoneal dialysis and haemodialysis may be used in gravidas with ARF. Early 'prophylactic' dialysis should be applied to pregnant women. Careful monitoring of fluid balance and anticoagulation is necessary during dialysis.

Thrombotic Thrombocytopenic Purpura

Thrombotic thrombocytopenic purpura (TTP) is classically highlighted by a pentad of features: fever, hemolytic anemia, thrombocytopenia purpura, transient or permanent central nervous system signs, and renal disease. The antemortem diagnosis is reliant upon the multisystem clinical signs and symptoms in conjunction with severe hemolytic anemia and thrombocytopenia. Relapse is common within the first six months after initial presentation. Laboratory findings have been generally nonspecific per se, and antemortem tissue biopsy findings are frequently unrewarding. Recently, however, unusually large multimers of the Factor VIII:Ag molecule (von Willebrand protein) have been identified in the plasma of patients with TTP who have recovered from an acute attack. This observation is very important because it may lead to essential information on the nature of the inciting event in this devastating illness. The differential diagnosis includes several multisystem disease processes such as the hemolytic uremic syndrome, toxemia of pregnancy, systemic lupus erythematosus, subacute bacterial endocarditis, nonbacterial thrombotic endocarditis, immune thrombocytopenic purpura, and the postpartum renal failure syndrome. The hemolytic uremic syndrome, toxemia of pregnancy, and TTP may resemble each other, exhibit many overlapping features, and are probably related. The cause of TTP remains unknown; the overwhelming majority of cases occur in otherwise healthy people without any recognizable underlying illness. Since 1965 45 to 70% of patients survive, a significant improvement in contrast to the early 1900s when the mortality rate was greater than 90%. The most dramatic advance has been observed in therapeutics, namely the utilization of some mode of plasma therapy (either infusion alone or plasmapheresis followed by plasma infusion). Corticosteroids remain very important in the management of patients with TTP. Vincristine may be very helpful, but additional studies are needed. The efficacy of vinca alkaloids, chronic immunosuppressive therapy, and sple. nectomy remains undefined. At present there is very little, if any, evidence that antiplatelet agents, aspirin, and prostacyclin are beneficial to patients with TTP. Prompt diagnosis and vigorous aggressive therapy is critical for successful management of TTP patients.

Postpartum Renal Failure

THE syndrome of postpartum renal failure, recognized since 1968, is an idiopathic condition characterized by renal failure in association with microangiopathic hemolytic anemia and, usually, thrombocytopenia occurring within a few days to approximately 10 weeks after an apparently normal pregnancy and delivery.1 , 2 This syndrome is regarded as distinct from acute renal failure occurring in the third trimester of pregnancy or within 48 hours of delivery because of obstetric complications, such as abruptio placentae, postpartum hemorrhage, amniotic-fluid embolism, puerperal sepsis, and eclampsia.3 Since the idiopathic condition is characterized by clinically overt symptoms occurring at least three or more days after an . . .

Hemodynamically mediated glomerular injury and the progressive nature of kidney disease

A 26-year-old woman was transferred to New England Medical Center (NEMC) from another hospital with a diagnosis of acute renal failure complicating antepartum hemorrhage, abruptio placentae, and shock. Emergency Caesarean section delivered a stillborn child 2 days prior to transfer. Postoperatively, the patient developed hypotension, oozing from the surgical site that required multiple transfusions, and acute oliguria. At NEMC, the patient remained oliguric for 16 days and was virtually anuric for the first 10 days; the 24-hr urine volumes averaged less than 50 cc. An abdominal x-ray revealed an 11.5-cm right kidney and a 12.5-cm left kidney. The BUN and serum creatinine levels rose as high as 128 and 18.9 mgldl. Hemodialysis was performed on three occasions during the period of oligoanuria. The urine output subsequently increased to a high of 1900 ml by the 29th hospital day. The patient was discharged 5 weeks after admission with a serum creatinine of 12.6 mg/dl. Over the next 6 months, the serum creatinine gradually declined to 4.9 mg/dl. Nine months after the episode of acute renal failure, percutaneous renal biopsy yielded only medullary tissue with nonspecific degenerative changes, a marginal focus of necrosis, and numerous protein casts. At this time, abdominal x-ray showed a 10-cm right kidney and an 11-cm left kidney. Over the next 3 years, the serum creatinine continued to decline gradually and finally reached 4.0 mgldl. During this period, urinary protein excretion ranged between 0.5 and 2 g/day. During this 3-year period, the patient also developed hypertension and was treated for the next 5 years with 750 mg/day of methyldopa. In addition she had recurrent episodes of right-sided paresthesias and blurred vision that resolved following the discontinuation of oral contraceptives. After she stopped taking the oral contraceptive, she developed amenorrhea and galactorrhea. Evaluation revealed low levels of FSH activity consistent with partial pituitary destruction; this problem presumably was sustained in the immediate postpartum period. After maintaining stable renal function (the serum creatinine was approximately 4.0 mgldl) for another 4 years (years 4 through 8 after the episode of acute renal failure), the serum creatinine slowly rose over the ensuing 7 years. Hypertension returned, concomitant with the further decline in renal function, and again was treated with methyldopa. During this period, 24-hr urinary protein excretion varied from 0.5 to 1.2 g. Uremic symptoms developed when the serum creatinine reached 8.7 mg/dl, 15 years after the acute postpartum renal failure, and chronic ambulatory peritoneal dialysis was initiated.

Acute Renal Failure in Pregnancy

Since the dramatic decrease in the incidence of septic abortion in industrialized countries, acute renal failure (ARF) complicating pregnancy represents a small percentage of the cases of acute renal shutdown, falling in France from 40% in 1966 to 4.5% in 1978 [1]. It is underlined in most series that the mortality rate in ARF associated with pregnancy is lower than that observed in nonobstetric ARF. In their recent survey, Cameron and Brown reported that it ranged from 9 to 34% [2]. This is probably explained by the young age of the patients and, in the most recent studies, also by the earlier detection of the underlying obstetric complications and their better management. Chapman and Legrain indicated that in the Department of Obstetrics at the Foch Hospital in Suresnes, France, no case of acute renal failure was observed among 12,000 delivered women, including 5 with eclampsia and 25 with abruptio placentae [1]. In their large study of 154 women with eclampsia, Pritchard and Pritchard noted only one case of ARF [3]. In contrast with these relatively optimistic data, ARF in pregnancy bears a high risk of bilateral renal cortical necrosis (BRCN), and consequently of chronic renal failure. In 1972, Kleinknecht et al found that the incidence of BRCN was 21% in postpartum renal failure, whereas it was only 1.5% in postabortum ARF. Among 38 cases of BRCN, 26 (68%) were of obstetric origin [4]. In addition to the classical renal complications of pregnancy, idiopathic postpartum ARF has been recognized for the last decade [5]. It often leads to irreversible renal failure and is associated with a high mortality rate. The pathogenesis of this syndrome remains to be elucidated, and its relationship to the idiopathic hemolytic uremic syndrome and thrombotic thrombocytopenic purpura is still debated [5]. The present review is based on the data in the literature and on our own experience with 57 cases of ARF related to pregnancy, referred to the Necker Hospital from 1957 to 1979 (including 47 cases after 1966). Some patients were included in a previous paper from our clinic [4]. Patients with septic abortion were excluded. The main clinical and pathologic features are summarized in Table 1. The circumstances leading to ARF are listed in Table 2. The overall maternal mortality rate was 14% (Table 2).

Acute renal failure in pregnancy

Since the dramatic decrease in the incidence of septic abortion in industrialized countries, acute renal failure (ARF) complicating pregnancy represents a small percentage of the cases of acute renal shutdown, falling in France from 40% in 1966 to 4.5% in 1978 [1]. It is underlined in most series that the mortality rate in ARF associated with pregnancy is lower than that observed in nonobstetric ARF. In their recent survey, Cameron and Brown reported that it ranged from 9 to 34% [2]. This is probably explained by the young age of the patients and, in the most recent studies, also by the earlier detection of the underlying obstetric complications and their better management. Chapman and Legrain indicated that in the Department of Obstetrics at the Foch Hospital in Suresnes, France, no case of acute renal failure was observed among 12,000 delivered women, including 5 with eclampsia and 25 with abruptio placentae [1]. In their large study of 154 women with eclampsia, Pritchard and Pritchard noted only one case of ARF [3]. In contrast with these relatively optimistic data, ARF in pregnancy bears a high risk of bilateral renal cortical necrosis (BRCN), and consequently of chronic renal failure. In 1972, Kleinknecht et al found that the incidence of BRCN was 21% in postpartum renal failure, whereas it was only 1.5% in postabortum ARF. Among 38 cases of BRCN, 26 (68%) were of obstetric origin [4]. In addition to the classical renal complications of pregnancy, idiopathic postpartum ARF has been recognized for the last decade [5]. It often leads to irreversible renal failure and is associated with a high mortality rate. The pathogenesis of this syndrome remains to be elucidated, and its relationship to the idiopathic hemolytic uremic syndrome and thrombotic thrombocytopenic purpura is still debated [5]. The present review is based on the data in the literature and on our own experience with 57 cases of ARF related to pregnancy, referred to the Necker Hospital from 1957 to 1979 (including 47 cases after 1966). Some patients were included in a previous paper from our clinic [4]. Patients with septic abortion were excluded. The main clinical and pathologic features are summarized in Table 1. The circumstances leading to ARF are listed in Table 2. The overall maternal mortality rate was 14% (Table 2).

Postpartum Hemolytic Uremic Syndrome

Three cases of postpartum hemolytic uremic syndrome (HUS) are presented. Symptoms of acute renal failure, hypertension and microangiopathic hemolytic anemia with thrombocytopenia occurred 10, 17 and 24 days after delivery. Despite early heparin therapy in all cases, one patient went into terminal renal failure needing chronic hemodialysis, with persistent hypertension which became uncontrollable requiring bilateral nephrectomy 6 months later. The second patient had diuresis one month after starting hemodialysis, but 3 months later developed malignant hypertension. Slight improvement in renal function with persistent hypertension occurred after hemodialysis for 20 months. The third patient showed complete clinical recovery after 2 months. Pathological examination of renal tissue showed the typical lesions of thrombotic microangiopathy (TMA). However, striking differences were observed in the lesion seen in early and late specimens. Early lesions could be differenciated from infancy TMA because the medium-dize arteries were more severely involved. Late lesions were variable, ranging from minor changes in glomeruli and blood vessels, via ischemic and sclerotic lesions in glomeruli with arteriolosclerosis, to the vascular and glomerular lesions seen in malignant nephrosclerosis. There was a good correlation between the renal pathology and the clinical outcome of the patients. HUS with renal TMA as a cuase of postpartum renal failure has been reported in 49 patients with a fatal outcome in 61%. The pathogenesis of the syndrome probably involves a primary endothelial damage. This causes local renal intravascular coagulation in the presence of the usual postpartum hypercoagulable state. This is shown by the presence of fibrin-fibrinogen in glomeruli and vessels, increased plasma fibrin degradation products, thrombocytopenia and lowered levels of coagulation factors. There is little hematological or pathological evidence fo disseminated intravascular coagulation or an immune-complex disease. Hypocomplementemia seen frequently is probably due to local C3 activation via the alternative pathway.

Postpartum Hemolytic Uremic Syndrome

POSTPARTUM hemolytic uremic syndrome (HUS) is a condition of obscure origin with grave prognostic implications. Of the 40 cases described to date, 80% of the patients have died, and 15% have required maintenance dialysis or renal transplantation. Only 5% have recovered, and all of these showed improvement within one month.1 We describe a patient with postpartum HUS and renal failure who recovered much later than previously reported, after more than a year of receiving maintenance dialysis. Report of a Case A 28-year-old woman (gravida 2, para 0) was admitted to the Prentice Women's Hospital at the 28th week of pregnancy because of mild hypertension and protein-uria. Her first pregnancy five years earlier was interrupted by a spontaneous abortion at 15 weeks. During the current pregnancy, she gained 11.4 kg during a seven-month period, and her blood pressure (BP) had increased from 110/60 to 150/70 mm Hg. Results of urinalysis