183
OPHTHALMICARTERYVELOCIMETRY (MEAN, SD)
baseline obtained before 16 weeks. The study was approved by the local ethical committee of Shimane Medical University, and srandardised informed consent was obtained from each patient. The subjects were examined sitting with gel placed directly on the closed eyelid. The examination was over within 5 min. The ultrasound beam is essentially parallel to the ophthalmic artery; rhus, the blood flow is depicted in red. Waveforms were recorded over three to five cardiac cycles. The frequency shift was automatically corrected for angle. Peak systolic velocities (PV), end-diastolic velocities (EV), time-averaged mean peak velocities AV), and pulsatility index (PI, [PV-EV]/AV) were calculated. Paired t, analyses of variance, and Neuman-Keuls multiple comparison tests were used. Comparisons for which p < 0-05 were
regarded as significant. There were no significant differences between left and right PV,
20
EV, AV, and PI in non-pregnant and pregnant women. Therefore, left and right values were combined, and there were no significant differences for any index between non-pregnant and pregnant women (table). The values in pre-eclampsia were significantly higher than those in both other groups; PI was significantly lower in
pre-eclampsia. Ophthalmic artery flow-velocity waveforms can be easily depicted during pregnancy with colour doppler imaging. Ophthalmic artery velocimetry may be a useful technique when attempting to assess peripheral circulatory dynamics and to monitor the effects of therapy in patients with pre-eclampsia. Department of Obstetrics and Shimane Medical University, Izumo 693, Japan
Gynecology,
TOSHIYUKI HATA DAISAKU SENOH KOHKICHI HATA MANABU KITAO
1 Erikson SJ, Hendrix LE, Massaro BM, et al. Color doppler flow
imaging of the normal and abnormal orbit. Radiology 1989, 173: 511-16. 2 Lieb WE, Cohen SM, Merton DA, Shields JA, Mitchell DG, Goldberg BB. Color doppler imaging of the eye and orbit. Arch Ophthalmol 1991; 109: 527-31. 3 Guthoff RF, Berger RW, Winkler P, Helmke K, Chumbley LC Doppler ultrasonography of the ophthalmic and central retinal vessels. Arch Ophthalmol 1991, 109: 532-36.
Accelerated progression of renal function loss after two pregnancies in a patient with
proteinuria SIR,-In some women with chronic glomerular disease, pregnancy may increase the rate of progression of renal function loss.’-’ Several factors have been suggested to predispose for such a pregnancy-induced progressive loss of renal function, such as the presence of renal failure and/or systemic hypertension before pregnancy.’We report a patient with normal renal function and blood pressure but with overt proteinuria, whose renal function loss progressively worsened after each of two pregnancies. A 20-year-old woman was diagnosed with peripheral oedema, proteinuria, and erythrocyturia. Protein in urine amounted to 5 g per day with a selectivity of 15% (IgG/albumin clearance). Serum albumin was 18 g/l. Renal function was normal (serum creatinine 80 µmol 1, creatinine clearance 97 ml/min, and glomerular filtration rate 101 ml/min). Blood pressure was 115/80 mm Hg. Renal biopsy revealed normal glomeruli, tubules, and interstitium; immunofluorescence showed modest IgM depositions along the glomerular basement membrane and in the mesangium. The
nephrotic syndrome responded only partly to corticosteroid therapy protem 2-3 g per day). During follow-up over 4 years, the patient was treated with a salt-restricted diet and hydrochlorothiazide 25 mg Protein in urine remained stable at 3-5 g per day. At age 26 she had an exacerbation of the nephrotic syndrome during her first pregnancy. At that time protein was 7 g per day with serum albumin 16 g 1, requiring several albumin infusions. Blood pressure was
24
28
32
patient’s age (yr) Course of reciprocal
serum
creatinine.
JTT.= pregnancy, o= reciprocal serum creatinine during pregnancy, and . = value before and after pregnancy. Regression line of reciprocal serum creatinine is drawn for non-pregnant values. Lis=lisinopril treatment.
Shading= proteinuria.
100/70 mm Hg and remained normal. Delivery was uncomplicated 39 weeks. After this pregnancy, proteinuria persisted (5-7 g per day), serum creatinine rose to 132 pmol/l, while blood pressure was normal. Symptomatic antiproteinuric treatment with an angiotensin-converting-enzyme inhibitor, lisinopril, was started at
but withdrawn after a year because of a desired second pregnancy. During the second pregnancy the nephrotic syndrome remained stable and no hypertension occurred. This pregnancy ended successfully in the 36th week. In the 2 years thereafter, creatinine clearance fell to 24 ml/min and proteinuria remained (5-7 g per day). Renal biopsy 1 year after the second pregnancy revealed severe focal segmental glomerulosclerosis. Because of the worsening of renal function we believed that both pregnancies could have influenced the natural course of renal function loss in this patient. We therefore analysed the rate of progression of renal function loss by linear regression analysis of reciprocal serum creatinine values over time (figure). After both pregnancies the slope of the regression line changed, indicating an accelerated progression of renal function loss. During both pregnancies hypertension did not occur although serum creatinine
decreased, probably indicating pregnancy-related hyperfiltration.3 Since our patient had no signs of renal failure or hypertension before the first pregnancy, factors other than those implied from previous reports may have a role. Because of the relation between proteinuria and progression of renal function loss,6 we propose that the presence of proteinuria before pregnancy may predispose for pregnancy-induced accelerated progression. Maintaining a reciprocal serum creatinine plot of such a patient is useful, since it may uncover whether a rise in serum creatinine happens in relation to pregnancy. Department of Nephrology, State University Hospital Groningen, 9713 EZ Groningen, Netherlands 1. Packham
MARC H. HEMMELDER DICK DE ZEEUW PAUL E. DE JONG
DK, North RA, Fairley KF, et al. Primary glomerulonephritis and QJ Med 1989; 266: 537-53. 2. Surian M, Imbasciatti E, Cosci P, et al. Glomerular disease and pregnancy. Nephron 1984; 36: 101-05. 3. Katz AI, Davison JM, Hayslett JP, et al. Pregnancy m women with kidney disease. Kidney Int 1980; 18: 192-206. 4. Imbasciatti E, Pardi G, Capetta P, et al. Pregnancy m women with chronic renal failure. Am J Nephrol 1986; 6: 193-98. 5. Hou SH, Grossman SD, Madias NE. Pregnancy in women with renal disease and moderate renal insufficiency Am J Med 1985; 78: 185-94. 6. Remuzzi G, Bertani T. Is glomerulosclerosis a consequence of altered glomerular permeability to macromolecules? Kidney Int 1990; 38: 384-94. pregnancy.
OPHTHALMICARTERYVELOCIMETRY (MEAN, SD)
baseline obtained before 16 weeks. The study was approved by the local ethical committee of Shimane Medical University, and srandardised informed consent was obtained from each patient. The subjects were examined sitting with gel placed directly on the closed eyelid. The examination was over within 5 min. The ultrasound beam is essentially parallel to the ophthalmic artery; rhus, the blood flow is depicted in red. Waveforms were recorded over three to five cardiac cycles. The frequency shift was automatically corrected for angle. Peak systolic velocities (PV), end-diastolic velocities (EV), time-averaged mean peak velocities AV), and pulsatility index (PI, [PV-EV]/AV) were calculated. Paired t, analyses of variance, and Neuman-Keuls multiple comparison tests were used. Comparisons for which p < 0-05 were
regarded as significant. There were no significant differences between left and right PV,
20
EV, AV, and PI in non-pregnant and pregnant women. Therefore, left and right values were combined, and there were no significant differences for any index between non-pregnant and pregnant women (table). The values in pre-eclampsia were significantly higher than those in both other groups; PI was significantly lower in
pre-eclampsia. Ophthalmic artery flow-velocity waveforms can be easily depicted during pregnancy with colour doppler imaging. Ophthalmic artery velocimetry may be a useful technique when attempting to assess peripheral circulatory dynamics and to monitor the effects of therapy in patients with pre-eclampsia. Department of Obstetrics and Shimane Medical University, Izumo 693, Japan
Gynecology,
TOSHIYUKI HATA DAISAKU SENOH KOHKICHI HATA MANABU KITAO
1 Erikson SJ, Hendrix LE, Massaro BM, et al. Color doppler flow
imaging of the normal and abnormal orbit. Radiology 1989, 173: 511-16. 2 Lieb WE, Cohen SM, Merton DA, Shields JA, Mitchell DG, Goldberg BB. Color doppler imaging of the eye and orbit. Arch Ophthalmol 1991; 109: 527-31. 3 Guthoff RF, Berger RW, Winkler P, Helmke K, Chumbley LC Doppler ultrasonography of the ophthalmic and central retinal vessels. Arch Ophthalmol 1991, 109: 532-36.
Accelerated progression of renal function loss after two pregnancies in a patient with
proteinuria SIR,-In some women with chronic glomerular disease, pregnancy may increase the rate of progression of renal function loss.’-’ Several factors have been suggested to predispose for such a pregnancy-induced progressive loss of renal function, such as the presence of renal failure and/or systemic hypertension before pregnancy.’We report a patient with normal renal function and blood pressure but with overt proteinuria, whose renal function loss progressively worsened after each of two pregnancies. A 20-year-old woman was diagnosed with peripheral oedema, proteinuria, and erythrocyturia. Protein in urine amounted to 5 g per day with a selectivity of 15% (IgG/albumin clearance). Serum albumin was 18 g/l. Renal function was normal (serum creatinine 80 µmol 1, creatinine clearance 97 ml/min, and glomerular filtration rate 101 ml/min). Blood pressure was 115/80 mm Hg. Renal biopsy revealed normal glomeruli, tubules, and interstitium; immunofluorescence showed modest IgM depositions along the glomerular basement membrane and in the mesangium. The
nephrotic syndrome responded only partly to corticosteroid therapy protem 2-3 g per day). During follow-up over 4 years, the patient was treated with a salt-restricted diet and hydrochlorothiazide 25 mg Protein in urine remained stable at 3-5 g per day. At age 26 she had an exacerbation of the nephrotic syndrome during her first pregnancy. At that time protein was 7 g per day with serum albumin 16 g 1, requiring several albumin infusions. Blood pressure was
24
28
32
patient’s age (yr) Course of reciprocal
serum
creatinine.
JTT.= pregnancy, o= reciprocal serum creatinine during pregnancy, and . = value before and after pregnancy. Regression line of reciprocal serum creatinine is drawn for non-pregnant values. Lis=lisinopril treatment.
Shading= proteinuria.
100/70 mm Hg and remained normal. Delivery was uncomplicated 39 weeks. After this pregnancy, proteinuria persisted (5-7 g per day), serum creatinine rose to 132 pmol/l, while blood pressure was normal. Symptomatic antiproteinuric treatment with an angiotensin-converting-enzyme inhibitor, lisinopril, was started at
but withdrawn after a year because of a desired second pregnancy. During the second pregnancy the nephrotic syndrome remained stable and no hypertension occurred. This pregnancy ended successfully in the 36th week. In the 2 years thereafter, creatinine clearance fell to 24 ml/min and proteinuria remained (5-7 g per day). Renal biopsy 1 year after the second pregnancy revealed severe focal segmental glomerulosclerosis. Because of the worsening of renal function we believed that both pregnancies could have influenced the natural course of renal function loss in this patient. We therefore analysed the rate of progression of renal function loss by linear regression analysis of reciprocal serum creatinine values over time (figure). After both pregnancies the slope of the regression line changed, indicating an accelerated progression of renal function loss. During both pregnancies hypertension did not occur although serum creatinine
decreased, probably indicating pregnancy-related hyperfiltration.3 Since our patient had no signs of renal failure or hypertension before the first pregnancy, factors other than those implied from previous reports may have a role. Because of the relation between proteinuria and progression of renal function loss,6 we propose that the presence of proteinuria before pregnancy may predispose for pregnancy-induced accelerated progression. Maintaining a reciprocal serum creatinine plot of such a patient is useful, since it may uncover whether a rise in serum creatinine happens in relation to pregnancy. Department of Nephrology, State University Hospital Groningen, 9713 EZ Groningen, Netherlands 1. Packham
MARC H. HEMMELDER DICK DE ZEEUW PAUL E. DE JONG
DK, North RA, Fairley KF, et al. Primary glomerulonephritis and QJ Med 1989; 266: 537-53. 2. Surian M, Imbasciatti E, Cosci P, et al. Glomerular disease and pregnancy. Nephron 1984; 36: 101-05. 3. Katz AI, Davison JM, Hayslett JP, et al. Pregnancy m women with kidney disease. Kidney Int 1980; 18: 192-206. 4. Imbasciatti E, Pardi G, Capetta P, et al. Pregnancy m women with chronic renal failure. Am J Nephrol 1986; 6: 193-98. 5. Hou SH, Grossman SD, Madias NE. Pregnancy in women with renal disease and moderate renal insufficiency Am J Med 1985; 78: 185-94. 6. Remuzzi G, Bertani T. Is glomerulosclerosis a consequence of altered glomerular permeability to macromolecules? Kidney Int 1990; 38: 384-94. pregnancy.
