Finally, although pregnancy-induced renal hyperiltration theoretically may impair long-term graft survival, Sturgiss and study of 34 allograft recipients followed for a mean of 15 years.
Others have reported similar findings (Debska-Slizien, 2014;
Stoumpos, 2016).
Close surveillance is necessary. Covert bacteriuria is treated, and if it is recurrent, suppressive therapy is given for the remainder of the pregnancy. Serial hepatic enzyme concentrations and blood counts are monitored for toxic efects of azathioprine and cyclosporine. Some recommend measurement of serum cyclo sporine levels. Gestational diabetes is more common if corti costeroids are taken, and overt diabetes must be excluded with tation. Surveillance for opportunistic infections from herpesvi rus, cytomegalovirus, and toxoplasmosis is important because these infections are common. Some recommend surveillance for BK virus, however, treatment is problematic Gosephson, 2011).
Renal function is monitored, and the GFR usually increases 20 to 25 percent. If a signiicant rise in the serum creatinine level is detected, then its cause must be determined. Possibilities include acute rejection, cyclosporine toxicity, preeclampsia, infection, and urinary tract obstruction. Evidence of pyelonephritis or graft rejection should prompt aggressive management. Imaging studies and kidney biopsy may be indicated. The woman is carefully monitored for development or worsening of underlying hypertension, and especially superimposed preeclampsia. Management of hypertension during pregnancy is the same as for patients without a transplant.
Because of increased incidences of fetal-growth restriction and preterm delivery, vigilant fetal surveillance is indicated (Chaps. 42, p. 814 and 44, p. 852). Although cesarean delivery is reserved for obstetrical indications, occasionally the transplanted kidney obstructs labor. In all women with a renal transplant, the cesarean delivery rate exceeds 60 percent (Bramham, 2013; Rocha, 2013).
This usually autosomally dominant systemic disease primarily afects the kidneys. The disease is found in 1 in 800 live births and causes approximately 5 to 10 percent of end-stage renal disease in the United States. Although genetically heterogeneous, almost 85 percent of cases are due to PD1 gene mutations on chromosome 16, and the other 15 percent to PD2 mutations on chromosome 4 (Zhou, 2015). Prenatal diagnosis is available if the mutation has been identiied in a family member or if linkage is established in the family.
Renal complications are more common in men than in women, and symptoms usually appear in the third or fourth decade. Flank pain, hematuria, proteinuria, abdominal masses, and associated calculi and infection are common. Hypertension develops in 75 percent, and progression to renal failure is a major problem. Superimposed acute kidney injury may also develop from infection or obstruction from ureteral angulation by cyst displacement.
Other organs are frequently involved. Asymptomatic hepatic cysts coexist in a third of patients with polycystic kidneys. Hepatic involvement is more common and more aggressive in women, and massive polycystic liver disease is almost exclusively found in multiparous women (Zhou, 2015). Approximately 10 percent of patients with polycystic kidney disease die from rupture of an associated intracranial bery aneurysm. Up to a fourth of patients have cardiac valvular lesions that involve valve prolapse or incompetence.