Thereafter, there is a steady return of blood pressure to pre-pregnancy levels until term. This increases the glomerular filtration rate GFR and gives rise to frequency and nocturia, resulting in decreased creatinine blood levels. The increased vascularity of the kidneys makes a renal biopsy beyond 32 weeks risky. Despite the increase in renal blood flow, the pressure within the glomerulus remains unaltered owing to compensatory effects on the afferent and efferent arteriole, but this only occurs in a normal kidney.
Any pre-existing disease in the kidney will be accelerated, often with deterioration in renal function. Pregnancy also affects the renal tubules. There is decreased reabsorption of glucose and bicarbonate, leading to glycosuria and bicarbonaturia. Despite the loss of bicarbonate, there is a persistent alkalosis owing to an increased respiratory rate.
There is hypercalciuria, although the risk of renal stones is not increased as inhibitors of stone formation also increase. Isolated pyuria is common and disappears by 3 months postpartum. Important renal adaptations in pregnancy. Estimating glomerular filtration rate in pregnancy. It has become a standard clinical method used to estimate renal function in patients with CKD. The use of this formula has not been well studied in the pregnant population and guidelines for its use exclude pregnant women, [2] because creatinine falls in pregnancy owing to a pregnancy-induced increase in GFR and haemodilution from plasma expansion.
This inaccuracy is more pronounced in pregnancy. Estimating proteinuria in pregnancy. Proteinuria needs to be measured first to monitor pre-existing proteinuria, which may increase substantially during pregnancy.
The protein-creatinine ratio PCR is the preferred method for quantitating proteinuria in the non-pregnant state [5] and its use is recommended to monitor pre-existing proteinuria during pregnancy. Specific diseases of the kidney. Hypertensive disorders, including pre-eclampsia. Hypertensive disorders of pregnancy are the commonest medical complications in pregnancy, and remain the most prevailing direct cause of maternal mortality in SA.
Pre-eclampsia appears to be initiated by abnormal implantation of the placenta, leading to hypoperfusion and ischaemia. There is accumulating evidence supporting the release of several placental anti-angiogenic factors including soluble fms-like tyrosine kinase sFlt1 and its synergist, soluble endoglin sEng. These anti-angiogenic factors are induced or exacerbated by placental ischaemia, with sFlt1 being a circulating antagonist to both vascular endothelial growth factor VEGF and placental growth factor.
When administered to pregnant rats, sFlt1 and sEng produce a syndrome resembling that of HELLP haemolysis, elevated liver enzymes, and low platelets. Clinically, vascular endothelial dysfunction and microangiopathy are present in the mother, but not in the fetus. The predominant target organ may be the brain seizures or eclampsia , the liver HELLP syndrome , or the kidney glomerular endotheliosis and proteinuria.
Predisposing factors include pre-existing hypertension, CKD, obesity, diabetes mellitus, thrombophilias, and multiple gestations. Screening for pre-eclampsia has the greatest impact on clinical outcomes, but to date there is no effective preventive treatment. Although two large meta-analyses have suggested a small, but significant, overall benefit in patients treated with aspirin, [20,21] the delivery of the fetus is currently the only definitive treatment.
Considerable evidence suggests that pre-eclampsia predisposes women to late cardiac and vascular diseases [22] and also increases the risk of subsequent CKD. The risk is greater if a pre-eclamptic pregnancy results in the birth of a low-birth-weight or preterm infant or if pre-eclampsia occurs in more than one pregnancy. Chronic kidney disease in pregnancy.
Women with CKD who become pregnant are at increased risk for adverse maternal and fetal outcomes, including a rapid decline in renal function, intrauterine grown retardation, perinatal mortality and pre-eclampsia. Obstetric outcomes are also partly related to the level of available neonatal care.
Very importantly, maternal renal function may decline irreversibly proportional to the level of pre-existing dysfunction.
In a SA setting, this is an important consideration as access to dialysis is limited in the state sector. Maternal renal function declines proportional to the level of pre-existing renal dysfunction [24,26]. The stress of increased renal blood flow and inability of the glomerulus to regulate intraglomerular pressure, which normally remains unaltered during pregnancy, may exacerbate renal damage in pre-existing disease. Managing dialysis and renal transplant patients.
CKD is generally characterised by menstrual disturbances and infertility, and is reversed by transplantation but not by dialysis. When pregnancy does occur, it needs to be co-managed by a nephrologist and an obstetrician as significant changes in management are required to improve maternal and neonatal outcomes. Transplant patients should also be co-managed as immunosuppressive drugs may need to be altered and their plasma levels will need to be carefully monitored. Pregnant women who have a transplanted kidney with renal dysfunction should be considered in the same way as other patients with CKD.
Pregnancy-induced acute kidney injury. Acute kidney injury AKI in pregnancy may be caused by any of the disorders leading to renal failure in the general population, e. There are, however, pregnancy-related complications characteristic of each trimester that can result in renal failure. In the second and third trimesters, pregnancy-specific conditions, e. At delivery, placental abruption can be associated with severe ATN and bilateral cortical necrosis.
The management of AKI is similar to that in a non-pregnant patient, with fluid management being especially important, particularly in the context of pre-eclampsia, as the vascular endothelium is very leaky.
Potential nephrotoxins such as the non-steroidal anti-inflammatory drugs NSAIDs and aminoglycosides should be used with caution throughout the pregnancy. Managing the complicated patient. Diabetic nephropathy is frequently encountered during pregnancy. Pre-pregnancy counselling is important, as obstetric and renal outcomes are determined by the degree of peripartum CKD. There is no increased risk of overt nephrophathy or end-stage renal disease in women with normal renal function at conception.
Women with lupus nephritis should be advised to conceive after a 6-month period of quiescent disease. There is also an increased risk of pre-eclampsia. Extra-renal disease flare-ups are more common in the second and third trimesters, and postpartum flare-ups have been described. Flare-ups can be managed with corticosteroids. Maintenance therapy with azathioprine and hydroxychloroquine is considered safe.
Tacrolimus and cyclosporin can be used in pregnancy with therapeutic drug level monitoring. Differentiating between a flare-up of lupus nephritis and pre-eclampsia may be challenging. Calcineurin inhibitors, glucocorticosteroids and azathioprine are the mainstay of safe immunosuppressive therapy in pregnant transplant recipients and lupus patients.
Mycophenolate mofetil has been reported to cause developmental toxicity, malformations, and intrauterine death in animals, with growing evidence confirming its teratogenic effects in humans.
The drug should be discontinued 6 weeks before conception. Because there are substantial physiological changes that occur in a normal pregnancy, it is necessary to understand these in order to determine whether the kidney developed disease during pregnancy.
Both pre-existing hypertension and renal disease increase the risk of adverse pregnancy outcomes and increase the risk of pre-eclampsia, which predisposes to preterm delivery. Pregnancy in a patient with CKD may cause progression of renal failure, and in the SA setting this is complicated by restricted access to dialysis in the state sector. To ensure the best outcome for mother and child, pre-pregnancy counselling is essential. Attention must be paid to the numerous teratogenic drugs that are commonly used to treat hypertension and the immunosuppression necessary to treat renal transplant recipients and those with glomerulonephritis e.
Patients with renal disease and hypertension are at high risk of complications and regular antenatal assessments are required that should involve a multidisciplinary team to monitor BP, proteinuria, diabetic control and fetal wellbeing.
Hydronephrosis during pregnancy: A literature survey. Levey AS. Use of glomerular filtration rate measurements to assess the progression of renal disease. Semin Nephrol ; Assessment of glomerular filtration rate during pregnancy using the MDRD formula.
Br J Obstet Gynaecol ; Estimation of glomerular filtration rate in preeclamptic patients. Am J Perinatal ; Am J Kidney Dis ; American College of Obstetricians and Gynecologists. Diagnosis and management of preeclampsia and eclampsia. Int J Gynaecol Obstet ; Use of protein: Creatinine ratio measurements on random urine samples for prediction of significant proteinuria. A systematic review. Clin Chem ; Renal disorders in pregnancy can range from asymptomatic bacteriuria to end-stage renal disease requiring dialysis, all being influenced by the physiologic changes of pregnancy.
Women who have mild to moderate renal disease or a renal transplant are now challenging obstetricians and nephrologists with pregnancy. Thus, these physicians must understand renal diseases and their effect on pregnancy, and vice versa. This chapter reviews the physiology of renal changes during pregnancy and provides a summary of renal disorders. Anatomic changes involving the urinary tract begin in the first trimester of pregnancy and can persist up to 16 weeks postpartum. These changes include dilatation of the renal calyces, pelves, and ureters, as well as reduced ureteral peristaltic activity.
Their precise etiology is unknown but can be attributed to a combination of mechanical and hormonal factors. In addition, there is reduced ureteral peristalsis and a greater volume of residual urine compared with the nonpregnant state. These factors predispose to urinary stasis and to an increased risk of infection. Much of the data relating to the effect of pregnancy on renal hemodynamics are derived from small studies in which measurements show considerable individual variation. Autoregulation maintains renal blood flow at a relatively constant level despite wide variations in perfusion pressure mean renal artery pressure.
Renal blood flow is usually assessed by p -aminohippurate clearance, which measures effective renal plasma flow ERPF. The ERPF significantly increases during pregnancy. The ERPF and glomerular filtration rate GFR in pregnancy are markedly affected by posture, being maximal when the pregnant woman lies on her side. Nitric oxide, endothelin, and relaxin may play a role in renal vasodilation in human pregnancy. Table 1. Physiologic Changes in Pregnancy.
Renal Increased renal size and volume Increased glomerular size? Dilation of collecting system Altered glomerular membrane porosity Ureteral smooth muscle hypertrophy Ureteral connective tissue hyperplasia. Increased cardiac output as early as week 5 of gestation Decreased systemic vascular resistance Decreased blood pressure until midpregnancy; rises thereafter. Mild respiratory alkalosis Decreased serum hydrogen ion Increased blood pH 7.
Decreased osmotic thresholds for vasopressin secretion and thirst Increased metabolic clearance rate Increased circulating vasopressinase Increased circulating levels of antinatriuretic hormones, especially mineralocorticoids, aldosterone, and desoxycorticosterone Increased plasma rennin substrate and PRA activity Increased serum atrial natriuretic peptide levels Increase renal kallikren excretion.
Tests of renal function in pregnancy must be interpreted in relation to the changes in plasma volume, glomerular filtration, and tubular reabsorption that normally occur with advancing gestation.
Many of the commonly used tests of function yield lower results in pregnancy than in the nonpregnant state. Consequently, values that may be regarded as normal in the nonpregnant state may well indicate renal dysfunction in pregnancy. Uric acid, blood urea nitrogen BUN , and serum creatinine levels are crude indices of renal function.
Upper normal limits of plasma uric acid levels are 5 to 5. The kidney and liver affect serum urea levels. The liver synthesizes urea, which is influenced by protein intake, metabolism, and hepatic function.
Urea reabsorption is by the kidneys and varies with hydration. Therefore, it is possible for renal function to be normal in the presence of an abnormal BUN or abnormal in the presence of a normal BUN. Relation between plasma level of urea nitrogen and rate of glomerular filtration. A similar relationship exists for serum creatinine.
Relation between functioning renal tissue and clinical signs of renal failure. The hour creatinine clearance is the best clinical measurement of GFR. In the final weeks of pregnancy, creatinine clearance usually declines to near nonpregnant levels. Error in the measurement of creatinine clearance in a pregnant woman can occur; the most common type of error is an incomplete hour urine collection. Accurate timed urine collection is particularly difficult in pregnancy because significant volumes of urine may remain in the dilated collecting system.
To avoid this error, patients should be well hydrated and should rest on their left side for 1 hour before starting and completing the hour urine collection. Despite these problems, creatinine clearance still remains the most useful measure of GFR in clinical practice.
Urinalysis is essentially unchanged during pregnancy. However, many variables can affect the results. Normal kidneys should be able to concentrate urine to a specific gravity of 1.
In pregnancy, posture affects urine concentration and specific gravity. Urine tends to be more dilute after a left lateral position is maintained compared with an upright position. Dipsticks exposed to air will give false-positive results for glucose and false-negative results for blood.
Proteinuria diagnosed on dipstick should be confirmed with a hour urine. The method of collection is very important when collecting a urine specimen. It is difficult for the woman to obtain a satisfactory clean voided specimen by herself, especially when she is far along in pregnancy. In addition, the specimen must be collected before the pelvic examination; it may be collected by the examiner while the patient is in the dorsal lithotomy position.
The diagnosis of renal disease in pregnancy should begin by taking a careful history and performing a thorough physical examination. Particular attention should be directed toward any history of renal disorders, proteinuria, hypertension, collagen vascular diseases, or glycosuria affecting either the patient or close relatives. Physical examination includes inspection of the optic fundi. Signs of uremia are usually a late feature in the natural progression of renal disease and indicate significant dysfunction.
Laboratory investigation begins with urinalysis of protein, glucose, ketones, specific gravity, and sediment. Glucosuria is usually detected with a glucose oxidase-impregnated dipstick. In pregnancy, the most common reasons for persistent glucose in the urine are physiologic glucosuria of pregnancy and diabetes.
However, the possibility of primary renal disease with renal glucosuria should be considered. Conventional screening for proteinuria uses a dipstick that is sensitive to albumin. Five percent of healthy adults exhibit postural proteinuria, a benign condition; this can be ruled out by comparing protein levels in the first voided urine with a specimen obtained after the woman was upright for several hours. False-positive results for protein can be due to concentrated urine, many white blood cells in the urine, or vaginal secretions with epithelial cells.
Fever, stress, and exercise can also cause transient proteinuria. Proteinuria in pregnancy should be evaluated using a hour urine collection and should not be considered pathologic until it exceeds to mg in 24 hours. Both increased after 20 weeks' gestation. Studies have shown that a 2-hour or hour collection of urine correlates with creatinine clearance and protein measured in a hour specimen.
The nephritic syndrome is characterized by greater than 3 to 3. In assessing the significance of proteinuria in pregnancy, the clinician should remember that increasing protein excretion with advancing gestation associated with known renal disease does not necessarily indicate significant progression of the disease. Examination of urinary sediment requires a fresh specimen, ideally the first voided morning specimen.
The presence of cells within a cast indicates that the cells came from the renal parenchyma. As a general guide, leukocyte casts are associated with infections or inflammatory processes, erythrocyte casts with glomerular disease, and fatty casts with nephrosis.
In addition, pyuria is a common finding in renal disease. White blood cells, casts, and pyuria may be present as reaction inflammation of the glomeruli or kidney substance.
Pyuria in the absence of casts may be due to infection anywhere in the genitourinary tract. Finally, the nephritic syndrome is characterized by the presence of doubly refractile fat bodies Maltese crosses , which are visible only under polarized light.
The role of renal biopsy in pregnancy is controversial. It is potentially dangerous, especially in the presence of hypertension. Further, it has been argued that the histologic changes of glomerular disease may be obscured by the changes from pregnancy itself.
In the largest study of pregnant women, Packham and Fairley 11 reported on renal biopsies and concluded that renal biopsy in the first two trimesters of pregnancy did not appear to be associated with an increased rate of complications, and in most women it provides a positive diagnosis for undiagnosed hematuria and proteinuria.
However, Kullner and coworkers 12 reported 4 hematomas in 15 antepartum biopsies and 3 hematomas in 3 postpartum biopsies; 2 of these patients required transfusion. The occurrence of complications is similar to the major complication rate of 2.
Perirenal hematomas, perirenal abscess, and sepsis were considered major complications Lindheimer and associates 14 reviewed the role of renal biopsy in pregnancy and believed that biopsy should be performed only if it would change management and should be postponed until after delivery.
Postpartum renal biopsy may be useful in determining the prognosis for patients with hypertension in pregnancy. In a study of 20 postpartum renal biopsies, Gaber and Spargo 15 could distinguish between patients with glomerular endotheliosis, a reversible lesion with no long-term sequelae, and focal glomerulosclerosis, which is not reversible and indicates underlying hypertensive disease with nephrosclerosis.
It is possible to categorize almost all renal problems in pregnancy using the information gained from a detailed history, urinalysis, BUN, creatinine level, and creatinine clearance. In certain patients, renal ultrasound may provide useful additional information, particularly if renal calculi or a tumor is suspected, but may be limited secondary to the pregnancy. Renal radiographs are rarely indicated in pregnancy and pose a radiation hazard to the fetus.
If they are necessary, limiting the number of films will minimize the risk to the fetus. Computed tomography scans may aid in the diagnosis of nephritic abscesses, and magnetic resonance imaging may be helpful to rule out tumor. Radiation exposure to the fetus should not exceed 5 rads. Cystoscopy can be performed for the usual indications. With the legalization of abortions and the use of antibiotics, the incidence of acute renal failure ARF in pregnancy has markedly decreased in developed countries secondary to a decrease in the incidence of septic abortions.
A further decrease is due to improvements in prenatal care, quick recognition of the condition, and initiation of treatment of abruptio placentae and preeclampsia. In industrialized countries, the rate of ARF is less than 0. The most common precipitating factor was hemorrhage, which included 13 cases of abruptio placentae. Severe preeclampsia or eclampsia accounted for 12 cases, and infection was the cause in 8 patients. Defined as a sudden decrease in renal function that results in retention of nitrogenous wastes, ARF can be classified as prerenal, intrinsic, or postrenal.
The causes of ARF are listed in Table 2. Prerenal conditions are the most common causes of ARF and usually result from inadequate perfusion of the kidneys.
Obstetric complications of ARF include hemorrhage from placenta previa, abruptio placentae, and uterine atony Table 3. ARF from renal hypoperfusion is usually reversible within 24 to 36 hours with volume replacement and correction of the underlying cause. Most of the deaths from ARF in pregnancy are due to the underlying disease rather than the renal failure itself.
Table 2. Table 3. Preeclampsia-eclampsia HELLP syndrome Severe peripartum hemorrhage Abruptio placentae Disseminated intravascular coagulation secondary to a prolonged fetal demise Uterine atony Uterine lacerations and perforations Uterine dehiscence of cesarean scar.
Chorioamnionitis Septic abortion Puerperal sepsis. Hyperemesis gravidarum Severe vomiting from pyelonephritis. Vascular hyperactivity with preferential cortical ischemia, diminished glomerular permeability, intraluminal obstruction, back leak of luminal contents across damaged tubular epithelium, and abnormalities in prostaglandin metabolism all have been demonstrated in ATN. There follows a recovery phase characterized by a marked diuresis; in most patients, normal renal function resumes.
In addition, ATN can occur for the same reasons in the gravida as it occurs in the nonpregnant patient. It is important to distinguish between extrarenal azotemia and acute parenchymal renal failure.
The former may result from congestive heart failure, hypovolemia, infection, trauma, hemorrhage, and urinary tract obstruction. Analysis of serum and urine samples may prove helpful if the diagnosis is not clear. In ARF, volume correction should always precede the use of diuretics, with the exception of mannitol , which is a volume expander and an osmotic diuretic. Mannitol may reduce swelling of the endothelial cells and thus improve renal blood flow.
If the patient is volume expanded and not hypotensive, then mannitol is contraindicated and furosemide is the diuretic of choice. During the oliguric phase, fluids should be restricted to avoid hypertension and pulmonary edema. Life-threatening hyponatremia, hyperkalemia, and acidosis may develop rapidly; thus, electrolyte and acid-base status must be carefully monitored. Dialysis is often the treatment of choice. During the diuretic phase of ATN, patients are at risk for electrolyte imbalance and hypovolemia.
ARF may be complicated by neurologic signs such as progressive lethargy, hyperreflexia, clonus, and a positive Babinski's sign. These signs disappear as renal function improves. Bacterial infection is a major risk and must be aggressively treated. Adequate nutritional status is important to combat infection, replace lost protein, and facilitate recovery of renal function. Standard recommendations include restriction of protein, sodium, and potassium; however, dietary requirements vary from patient to patient and according to the level of renal function.
One of the benefits of dialysis is that it allows a more flexible diet. The condition is characterized by the death of renal cortical tissue with sparing of the medulla. Its pathophysiology is uncertain. Lindheimer and colleagues 21 suggested that endothelial damage by endotoxin is followed by the formation of thrombi. The incidence of BRCN is probably underestimated because patchy cortical necrosis with partial or almost complete recovery or renal function may be overlooked if a patient survives and the appropriate investigations are not undertaken.
Abruptio placentae is the most common pregnancy complication associated with BRCN, whereas the incidence is relatively low in patients with severe preeclampsia. BRCN should be strongly suspected if ARF develops before 30 weeks of gestation and is associated with prolonged anuria or oliguria of more than 10 days' duration.
Anuria or oliguria is the rule, and urine is usually blood-stained. Renal biopsy or selective arteriography can be used to confirm the diagnosis and distinguish between extensive and patchy cortical necrosis.
Most patients with BRCN progress to chronic renal failure; before the availability of renal dialysis, the condition was usually fatal. Some patients with this disease have a slow recovery in renal function for up to 3 years after the onset and can achieve a satisfactory lifestyle without dialysis. Preeclampsia is a syndrome characterized by hypertension and proteinuria. The disease process starts far before the appearance of any clinical signs or symptoms. Its etiology is unknown but is thought to be due to endothelial damage.
A multisystem disorder, preeclampsia has multiple effects on the kidney. It is a frequent cause of proteinuria in pregnancy. Endotheliosis, swollen intracapillary endothelial cells in the glomeruli, is the hallmark lesion of preeclampsia in the kidney.
In addition, preeclampsia may cause focal glomerular sclerosis. An increase in renal vascular resistance causes a reduction of renal blood flow. The exact etiology for the decline in renal function is unknown.
After delivery, the functional decrements usually reverse quickly but can progress to ATN if treatment is not initiated at an appropriate time. Pregnancy outcomes complicated by preeclampsia and ARF are associated with high rates of morbidity and mortality. Sibai and colleagues 18 reported outcomes in 31 pregnancies in 30 patients with renal failure; 18 women had preeclampsia and 12 had superimposed preeclampsia with existing hypertension, renal disease, or both.
All the women in the preeclampsia-only group developed ARF 1 to 5 days postpartum, whereas seven women in the other group developed ARF postpartum.
Overall, gestational age at delivery was less than 30 weeks in All 18 patients in the preeclampsia-only group had ATN, and 9 required dialysis. All patients had normal renal function within 8 weeks of follow-up. Two patients in this group died at 8 to 9 weeks postpartum after the ATN resolved. Autopsy results showed no residual renal disease.
In the other group, 11 patients survived and 9 of these patients required dialysis. Before delivery, seven of the nine had abnormal renal function. One patient who had glomerulosclerosis and ARF died 3 days after termination of her pregnancy at 16 weeks' gestation. The association of HELLP hemolysis, elevated liver enzymes, and low platelets syndrome complicated by acute renal failure does not significantly increase maternal morbidity or mortality rates.
Selcuk and colleagues 23 described 39 cases of pregnancy-related ARF. Recovery rate, maternal death rate, and fetal death rate were similar in both groups. There were no maternal deaths. An additional study revealed that subsequent pregnancies in patients who have had prior pregnancies complicated by ARF and HELLP syndrome tend to have favorable outcomes and long-term prognosis.
In conclusion, ARF is infrequent in well-managed patients with severe preeclampsia. Maternal and perinatal mortality and morbidity rates increase with the association of ARF in these patients. Early identification and proper management of ARF in patients without associated medical or obstetric complications does not result in residual renal damage. Chronic renal failure is defined as a reduction of renal mass and loss of renal reserve from an insult to the kidney.
Initially, surviving nephrons hypertrophy in number and function. This initial adaptation predisposes the remaining nephrons to sclerosis and unrelenting destruction, which can eventually lead to end-stage renal disease. Chronic renal failure has multiple etiologies; diabetes and hypertension have replaced glomerulonephritis as a major etiology.
Renal insufficiency is classified as mild, moderate, or severe. Patients with mild disease have a serum creatinine level of 1. Those with moderate renal insufficiency have a serum creatinine level of 1. Likewise, the effects of pregnancy do not worsen renal function when mildly impaired.
Early studies have reported a significant deterioration of renal function in pregnant patients with moderate renal insufficiency. However, more recent studies have shown less deterioration. In this study, end-stage renal disease was defined as a serum creatinine level of more than 6. Women with hypertension and renal disease at the first prenatal visit were not at increased risk for preterm delivery, IUGR, or reduced fetal survival.
However, hypertension in the third trimester was associated only with an increase in the rate of IUGR. Women with end-stage renal disease rarely become pregnant secondary to infrequent and irregular menstrual cycles, anovulation, and hormonal abnormalities.
The frequency of conception has been reported to range from 0. In addition, pregnancies may go unrecognized: early spontaneous abortion may be mistaken for heavy menses in women with end-stage renal disease with irregular menstruation. Okundaye and colleagues 33 reported the largest registry of pregnant patients with end-stage renal disease. In dialysis centers, pregnancies occurred in women.
In these women, 58 were started on dialysis after conception and conceived while undergoing dialysis. The outcome in women who conceived before dialysis was better than in those who conceived after beginning dialysis. Seventy-three percent of women who started on dialysis after conception had surviving infants, compared with The remaining The authors also concluded that a lower frequency of prematurity and low birthweight was associated with conception before dialysis.
There was no statistical significance between the fetal survival rate and causes of renal failure. In addition, women who had fewer years of dialysis before conceiving tended to have a better outcome compared with those with more years of dialysis. Lastly, there was no statistical difference in infant survival or mean gestational age of live-born infants among women with different frequencies of dialysis.
However, women who received more than 20 hours of dialysis per week had better infant survival rates and less prematurity than those receiving less than 20 hours per week. Of these, 4 infants died shortly after birth from prematurity and the other 11 showed normal development at 1 year of age.
One infant was diagnosed with retrolental fibroplasias of prematurity. There were no congenital anomalies. All showed signs of preterm labor and most were born prematurely, with the mean gestation age at delivery in the 11 surviving neonates of Survival of the neonate was associated with years of dialysis.
Neonates who died of prematurity were born to women who had been receiving dialysis for more than 9 years, and the remaining who survived were born to women who had been receiving dialysis for less than 6 years.
Dialysis management in a pregnant patient differs slightly from that in a nonpregnant one. During dialysis, it is important to avoid hypotension and rapid fluctuations in intravascular volume. Anemia is common in patients receiving dialysis and is exacerbated by pregnancy. Giving packed red blood cells during dialysis prevents volume overload and aggravation of hypertension.
Erythropoietin has been shown to be effective in treating anemia in pregnancy. In addition, patients receiving dialysis need a diet consisting of 70 g protein, mg calcium, 50 mmol potassium, and 80 mmol sodium, with supplements of dialyzable vitamins. Further, patients should be aware that they will have to contend with a high risk of pregnancy complications and an increased frequency and duration of dialysis.
Chronic renal failure is often accompanied by amenorrhea, but fertility returns rapidly after transplantation. During the past decade there has been a steady increase in the number of pregnancies after renal transplantation. Davison and Milne 36 reviewed pregnancies in transplant patients.
The incidence of graft rejection appears to be no greater than in the nonpregnant population. Infection is an important consideration in any patient receiving immunosuppressive drugs. Aseptic technique should be used for even minor surgery and steroid therapy augmented. A transplanted kidney rarely obstructs labor, and delivery by cesarean section is required only for obstetric reasons.
In utero exposure to high-dose steroid and immunosuppressive agents does not seem to be associated with an increased incidence of congenital anomalies in the offspring of pregnant women with a renal transplant. Current data suggest that steroids and immunosuppressive agents prednisone , cyclosporin A, and azathioprine at the doses used to prevent graft rejection in transplant recipients are well tolerated by the fetus.
In theory, these drugs could cause fetal growth retardation, adrenal and bone marrow suppression, and immunosuppression predisposing to intrauterine infection. Long-term studies are required to determine whether there may be other effects, particularly an increase in the incidence of malignancies or abnormalities in the subsequent generation. Before any woman with a renal transplant embarks on a pregnancy, an obstetrician and nephrologist should counsel her.
Lindheimer and colleagues 37 proposed guidelines for transplant patients before pregnancy. At least 2 years should have elapsed since the transplant, and the woman should be in good health without severe hypertension, severe renal insufficiency, or persistent proteinuria.
In addition, she should be receiving maintenance doses of immunosuppressive therapy. Pregnancy appears to have no effect on graft function or survival; however, an important concern is that a mother may not survive long after the pregnancy. Acute glomerulonephritis the acute nephritic syndrome is characterized by the abrupt appearance of red blood cells and red blood cell casts in the urine.
Renal function is usually impaired, with sodium and water retention leading to edema and hypertension. The BUN and creatinine levels rise, and creatinine clearance declines. Proteinuria is common but is normally less than 3. Renal diseases presenting as acute glomerulonephritis include poststreptococcal glomerulonephritis, lupus glomerulonephritis, membranoproliferative glomerulonephritis, and Goodpasture's syndrome.
Laboratory investigations may help to distinguish the different causes and should include urine microscopy, creatinine clearance, hour urinary protein collection, serum IgA and complement determinations, streptozyme assay and antistreptolysin 0 titers, and evaluation of antinuclear antibody.
Uremia may not respond to conservative measures and may require renal dialysis. Chronic glomerulonephritis implies progressive loss of renal function, proteinuria, and diminishing renal size caused by primary or secondary glomerular disease that has failed to resolve or respond to treatment.
End-stage renal failure eventually ensues, requiring hemodialysis. Jungers and associates 39 observed pregnancies in women with biopsy-proven primary chronic glomerulonephritis and concluded that pregnancy did not adversely affect the course of renal disease in patients who had normal renal function before pregnancy. Acute poststreptococcal glomerulonephritis is very uncommon in pregnancy. The diagnosis usually depends on a history of streptococcal infection within the previous weeks and an elevated antistreptolysin titer.
Fetal loss is almost invariable. Renal function returns to normal after delivery. Patients who have a history of poststreptococcal glomerulonephritis and whose renal function has returned to normal are not at risk of fetal loss or preeclampsia. In most countries, mesangial IgA nephropathy is the most common type of glomerulonephritis, and yet there are surprisingly few accounts of pregnancy and IgA nephropathy.
Kincaid-Smith and Fairley 41 summarized the outcome of pregnancies in 65 patients with mesangial IgA nephropathy. The outcome in individual patients with IgA nephropathy may vary from no change in renal function or biopsy features during 25 years to a fulminating progression to end-stage renal failure in a matter of 2 months.
It is therefore difficult to be certain whether renal function that deteriorates during pregnancy was precipitated by the pregnancy or was the natural course of the disease. The prognosis for fetal outcome is generally good in patients with normal renal function and without pre-existing or early developing hypertension.
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