Renal Disease

Davison, John M.; Baylis, Christine

doi:10.1002/9780470752371.ch7

Cited by 13 publications

(23 citation statements)

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“…39 Providing that the preconception serum creatinine is < ~1.4 mg/dL and that hypertension and/or heavy proteinuria are absent, the obsterical outcome, in terms of a healthy baby, is good. 35 The pattern is quite similar in women with renal disease secondary to type 1 diabetes, who usually also show a gestational rise in GFR, providing that the renal function is near normal preconception. 40 With more severe diabetic nephropathy, abrupt falls in GFR can occur during the pregnancy.…”

Section: Glomerular Hemodynamics During Compromised Pregnanciesmentioning

confidence: 93%

“…For instance, the incidence of preeclampsia is elevated, and in some situations, the superimposition of pregnancy has been reported to accelerate the rate of loss of renal function. 35 What predicts those women with CRD who are at risk for pregnancy-induced complications? Women with a variety of mild underlying primary renal diseases (serum creatinine <1.4 mg/dL) often show increases in GFR during pregnancy (Fig 5), although of smaller magnitude than seen in normal pregnant women.…”

Section: Glomerular Hemodynamics During Compromised Pregnanciesmentioning

confidence: 99%

“…54 Although severe loss of renal function compromises fertility, conception can occur, even in women with end stage renal disease who are on dialysis. In this population, the chances of a live birth are only ~20% to 50% and there is a risk of severe maternal consequences, particularly, uncontrolled hypertension, 35,55 Women with type 1 diabetes respond similarly to those with primary renal disease in terms of the impact of pregnancy on long-term renal function. When there is minimal renal impairment before conception (serum creatinine <1.4 mg/dL = 124 μmol/L), it is generally considered that pregnancy does not influence the course of diabetic nephropathy.…”

Section: Long-term Effects Of Pregnancy On the Kidney When Maternal Rmentioning

confidence: 99%

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confidence: 99%

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Impact of Pregnancy on Underlying Renal Disease

Baylis

2003

Advances in Renal Replacement Therapy

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Normal pregnancy involves marked renal vasodilation and large increases in glomerular filtration rate (GFR). Studies in rats reveal that the gestational renal vasodilation is achieved by parallel reductions in tone in afferent and efferent arterioles so GFR rises without a change in glomerular blood pressure. There is some evidence from animal studies that increased renal generation of nitric oxide (NO) may be involved. Although chronic renal vasodilation has been implicated in causing progression of renal disease in nonpregnant states by glomerular hypertension, there are no longterm deleterious effects of pregnancies on the kidney when maternal renal function is normal because glomerular blood pressure remains normal. When maternal renal function is compromised before conception, there are no long-term adverse effects on renal function in most types of renal disease, providing that the GFR is well maintained before conception. When serum creatinine exceeds ~ 1.4 mg/dL, pregnancy may accelerate the renal disease increases and when serum creatinine >2 mg/dL, the chances are greater than 1 in 3 that pregnancy will hasten the progression of the renal disease. The available animal studies suggest that glomerular hypertension does not occur despite diverse injuries. Thus, the mechanisms of the adverse interaction between pregnancy and underlying renal disease remain unknown. Index WordsGlomerular filtration rate; renal vasodilation; animal models; primary glomerular disease; diabetes There are profound hemodynamic changes in normal pregnancy including increases in plasma volume, red blood cell volume, and hence blood volume. Both stroke volume and heart rate increase leading to ~40% elevations in cardiac output, despite which, blood pressure (BP) falls because of large reductions in total peripheral vascular resistance (TPVR). [1][2][3] In addition to peripheral vasodilation, a vascular refractoriness to a variety of administered vasoconstrictors including angiotensin II develops quite early. [2][3][4] Striking changes also occur in kidney function, with an early increase in glomerular filtration rate (GFR), which is first detectable within 3 to 4 weeks after conception (Fig 1). 5 GFR continues to rise to a maximum of 40% to 50% above nonpregnant values by the end of the first trimester, and this increase is maintained throughout most of the pregnancy, although a fall in GFR occurs in the few weeks before delivery. 6 An optimal increase in GFR is a good prognosticator for a successful pregnancy outcome. As shown in Figure 1, in a serial study of normal pregnant women, 2 women who failed to show the early rise in GFR subsequently underwent early spontaneous abortion. 5 The rat is an excellent animal model for study because it exhibits systemic and renal hemodynamic changes during normal pregnancy that are similar to humans and the total gestation period in rats is only 22 days (Fig 2) volume expansion (which can reach 100% above the nonpregnant rat value) followed by a fall in blood pressure (although this is...

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Section: Glomerular Hemodynamics During Compromised Pregnanciesmentioning

confidence: 93%

Section: Glomerular Hemodynamics During Compromised Pregnanciesmentioning

confidence: 99%

Section: Long-term Effects Of Pregnancy On the Kidney When Maternal Rmentioning

confidence: 99%

mentioning

confidence: 99%

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Impact of Pregnancy on Underlying Renal Disease

Baylis

2003

Advances in Renal Replacement Therapy

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“…Pregnant women with CKD are at increased risk of pre-eclampsia, fetal loss, premature delivery, and long-term deterioration in renal function, and the risk is higher with moderate or severe renal disease than with mild disease 15 , 16. Ideally, young women with known kidney disease should be assessed prior to pregnancy, so that blood pressure and other potential risk factors can be optimised to help to achieve a successful outcome.…”

Section: About Ckdmentioning

confidence: 99%

The patient, the drug and the kidney

2006

DTB

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Recent policy changes have focused attention on the prevalence of chronic kidney disease (CKD) in the UK.1–3 In particular, automatic reporting of estimated glomerular filtration rate (e-GFR) is a requirement of the National Service Framework (NSF) for Renal Services in England.1 Also, the Quality and Outcomes Framework (QOF) of the UK General Medical Services (GMS) Contract (revised in April 2006) requires GPs to keep a renal register of patients with CKD with e-GFRs below 60mL/min/1.73m.2,4 Prescribers managing such patients are faced with difficult decisions about starting or continuing treatment with drugs that are handled by, or potentially toxic to, the kidney.4 Here we review methods of identifying and classifying CKD in adults and the implications of CKD for patients' health. We also offer advice on prescribing for these patients while minimising the risks of drug-related renal toxicity. We do not aim to give detailed guidance on every drug, but rather to highlight general principles of drug therapy and key sources of information and advice.

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In utero exposure to mycophenolate mofetil: A characteristic phenotype?

Pérez-Aytés

Lédo

Bosó

et al. 2007

American J of Med Genetics Pt A

147

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Mycophenolate mofetil (MMF) is a widely prescribed immunosuppressive agent after solid organ transplantation. Potential teratogenic effects after in utero exposure to MMF in experimental studies and clinical observations in humans has been postulated in recent literature. However, a specific pattern of malformation has not been identified yet. We present a newborn patient, born to a recipient of renal transplantation, who became pregnant while taking MMF as immunosuppressive therapy. The newborn exhibited cleft lip and palate, bilateral microtia and atretic external auditory canals, chorioretinal coloboma, hypertelorism, and micrognathia. An extensive review of the literature documented six other cases with similar malformations after in utero exposure to MMF. A consistent pattern of malformations comprising cleft lip and palate, microtia and external auditory canals could be observed in five of the six cases. A different malformative pattern observed in one of the patients could be attributed to a different agent rather than MMF. The possible teratogenic effects of other immunosuppressive drugs, such as tacrolimus and prednisone, to which this patient was also exposed, are discussed herein. In addition, the differential diagnosis with other dysmorphic syndromes that can present with a similar phenotype, such as CHARGE syndrome, 18q deletion and hypertelorism-microtia-clefting (HMC) syndrome, is presented. We conclude that in utero exposure to MMF can cause a characteristic phenotype and propose the existence of a mycophenolate-associated embryopathy whose main features are: cleft lip and palate, microtia with atresia of external auditory canal, micrognathia and hypertelorism. Ocular anomalies, corpus callosum agenesis, heart defects, kidney malformations, and diaphragmatic hernia may be part of the phenotypic spectrum of MMF embryopathy. The human teratogenicity of MMF is reinforced by this report, and the current contraceptive recommendations about its use in fertile women are stressed.

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Renal Disease

Cited by 13 publications

References 356 publications

Impact of Pregnancy on Underlying Renal Disease

Impact of Pregnancy on Underlying Renal Disease

The patient, the drug and the kidney

In utero exposure to mycophenolate mofetil: A characteristic phenotype?

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