Patient list


  • My first patient had SIADH and a sodium of 125
  • My last patient had nephrogenic diabetes insipidus and a sodium of 150
The statistician in me, looked at the patient list and concluded, normal sodium.

Lecture on how to give a lecture

This post really resonates with me: The Ten Commandments of PowerPoint and I wish that I had included it in my lectuer from last week on how to give a lecture.

The chief resident at St John Hospital and Medical Center asked me to do morning report on giving better presentations. It was an interesting project. I have been pretty busy and didn’t have enough time to put together a really polished presentation, but this is what I came up with.

Here is a link to the PDF and Keynote file (130 mb)

iWork documents are a little wonky if you are not using Safari. So the videos I embedded in the lecture are below if you are having trouble looking at them.

Steve Jobs tells it how it is regarding Microsoft

The birth of a morning report:

Screen captures with command-shift-4:

Smart builds

Highlight text:

Mask an image

Improve a crappy figure:

When the GFR is zero how fast does the creatinine rise?

How do you get a GFR of zero?
Bilateral bathtub nephrectomy

In my clinical experience when the GFR approaches zero the creatinine goes up between 1 and 2 mg/dL everyday.

However ai was working out a story problem for an acute renal failure and when I calculated how much the creatinine would rise it was 3.3 per day. Here is how I calculated this:

  • Total body creatinine: 420 mg
    • This assumes that creatinine is equally distributed through out total body water. So 42 liters (60% of 70kg) times 1 mg/dl times 10 dL per liter
  • New creatinine: 1400 mg
    • 20 mg of creatinine generation per kg body weight, 70 kg body weight
  • New total total body creatinine 1820 mg
    • add the first two figures
  • New creatinine: 4.33 mg/dL
    • Divide the total body creatinine (1820 mg) by total body water (420 dL):

Did I do my calculation wrong? The total body creatinine calculation of 420 mg seems awfully low, especially if muscles create 1400 mg of new creatinine everyday.

Picture by The Doctr

Index of my posts on membranous nephropathy, renal biopsy and pregnancy

  • The Question: When do you biopsy pregnant patients? A review of Clara Day’s NDT article on renal biopsy in pregnancy.

  • The Survey: Request for doctors to share their practice patterns on decision making regarding pregnant patients with renal disease.

  • The Plea: Request for more participants in the survey practice patterns.
  • The Research: a long, somewhat unstructured, bibiography of the literature.

  • The Conclusions: A summary of my findings and conclusions. This includes the results of the survey.

Membranous nephropathy and pregnancy

I promised a full examination of the renal biopsy in pregnancy.

This is the longest post I have ever done and so I have segmented it into two parts:

  1. My conclusions along with  discussion of the survey of clinical decision making
  2. The supporting data, which is structured as a detailed annotated bibliography.

My conclusions:

The renal biopsy is as safe in pregnancy as it is outside of pregnancy. Ultrasound guidance and modern understanding of coagulopathy paired with aggressive use of antihypertensives makes this an acceptable risk in pregnancy.  This is a field of medicine that accepts risk to the fetus to in the name of better diagnostic data, see amniocentesis.

As long as the blood pressure is controlled, and the patient is not coagulopathic, if you need the biopsy, get the biopsy.

However, I have not been fully satisfied that the diagnostic data is that useful in most situations. The therapeutic options in pregnancy seem pretty narrow:

  • IV methylprednisolone with or without azathioprine
  • Therapeutic abortion
  • Delivery of the infant prematurely
  • Symptomatic therapy

Given those options, a biopsy will not make a difference in many situations.

Timing becomes critical as a therapeutic abortion and delivery of the infant both have narrow windows of opportunity. The decision to use symptomatic treatment will not be influenced by histologic findings.

That leaves IV methylprednisolone. In every case report I read where methylprednisolone +/– azathioprine was used I thought the decision to use it coud have been made solely from the patient’s symptoms and that the biopsy results didn’t really influence that decision. In every case the mother had increasing blood pressure, creatinine and proteinuria 20+ weeks into the pregnancy. It was too early to deliver the baby and steroids were used to buy time for the fetus to grow prior to delivery.

Here are the situations I would recommend doing a biopsy:

  • First trimester with early signs that the patient may be in for a rocky pregnancy due to renal disease. There are three risk factors: nephrotic range proteinuria, renal failure with a creatinine over 1.5 and hypertension. Getting a pathologic diagnosis at this point could allow termination of the pregnancy if any frightening diagnosis are made, i.e. lupus nephritis, scleroderma, crescentic GN, possibly MPGN. Outside of those findings I doubt the biopsy will actually change your therapy. I am sympathetic to the argument that each of these diagnosis has pretty good serologic tests that could decrease the need for the biopsy. That said the decisions are weighty enough that I would prefere a tissue diagnosis.
  • The only other situation would be a patient with symptoms suggestive of scleroderma presenting late in pregnancy, 20+ weeks with high blood pressure. The right choice here is probably terminating the pregnancy. The mother’s life is in danger and the condition will not respond to steroids, the only therapeutic option available. I would like to get a tissue diagnosis to confirm prior to proceeding down that road.

In the survey I presented I had 6 different clinical scenarios, they are summarized below:

  1. Gestational age 12 weeks, nephrotic syndrome, normal BP, normal Cr
  2. Gestational age 24 weeks, nephrotic syndrome, normal BP, normal Cr
  3. Gestational age 12 weeks, nephrotic syndrome, normal BP, elevated Cr
  4. Gestational age 24 weeks, nephrotic syndrome, normal BP, elevated Cr
  5. Gestational age 12 weeks, nephrotic syndrome, elevated BP, elevated Cr
  6. Gestational age 24 weeks, nephrotic syndrome, elevated BP, elevated Cr
So I would recommend a biopsy in case 3 and 5, and think long and hard about case 1. I wouldn’t biopsy 2, 4 or 6. I would start steroids in case 6 and consider it in case 4. I didn’t vote this way, as my opinions have changed the more I learned and thought about this. Of note, the only maternal-fetal medicine doctor voted exactly as I just described. 
As of Sunday April 3rd we had 53 votes:
81% are nephrologists. I guess we know who reads PBFluids.
And 76% are from North America. And that compares favorably to the overall traffic to the blog:
from Google Analytics
Mexico represents 0.8% of blog traffic but showed up big time for 4% of the sample.
Here is how the community voted:
  1. Gestational age 12 weeks, nephrotic syndrome, normal BP, normal Cr.
    I voted BIOPSY, the community:

  2. Gestational age 24 weeks, nephrotic syndrome, normal BP, normal Cr.
    I voted NO biopsy, the community:
  3. Gestational age 12 weeks, nephrotic syndrome, normal BP, elevated Cr.
    I voted BIOPSY, the community:
  4. Gestational age 24 weeks, nephrotic syndrome, normal BP, elevated Cr.
    I voted NO biopsy, the community:
  5. Gestational age 12 weeks, nephrotic syndrome, elevated BP, elevated Cr.
    I voted BIOPSY, the community:
  6. Gestational age 24 weeks, nephrotic syndrome, normal BP, elevated Cr.
    I voted NO biopsy, the community:

The thing that confuses me is why the percent of people that want a biopsy at 12 weeks seems to fall as the patient gets sicker: 49% in case 1 to 34% in cases 3 and 5. What happened to 8 of the pro-biopsy doctors?

The same puzzling trend held for the 24 week gestational age with the biopsy rate being highest, 81%, in the healthiest and as the patient developed decreased renal function and hypertension it fell to 64% and 57%.

I broke down the data for attendings versus fellows:

And now you can see where those missing biopsies for the patient at 12 weeks went. Over half the fellows were willing to biopsy the asymptomatic nephrotic syndrome at 12 weeks. But the bravado disappeared if you added a bit of hypertension (scenario 3) with the biopsy rate falling below 20%.

The attendings were more likely to biopsy the patient in just about every scenario with an overall biopsy rate of 59% versus 49% for fellows.

In the U.S. versus the world:

It looks like a general trend for doctors outside of the US to be less likely to biopsy patients, at least in the first trimester.
Here is a link to the raw data in case anyone is interested. And yes I did see the fellow from Lebanon double voted, but given the importance of Chicago in the study of both renal disease in pregnancy and glomerular disease, I figured a vote early, vote often policy was appropriate.
Look here for the link to the second post with the annotated bibliography.

Renal Disease in Pregnancy, an annotated bibliography

Here’s an article on a placental site tumor resulting in secondary membranous nephropathy. More a curiosity than truly relevent as the diagnosis was made after delivery.

Also don’t forget the review of renal biopsy in pregnancy I did a week ago. I reviewed this article.

Sebestyen presents an interesting case. The patient first presented with proteinuria during her third trimester and undergoes a cesarian section at 36 weeks due to pre-eclampsia. At the time she had 3 grams of proteinuria on a 24-hour sample and a blood pressure of 170/100. Six weeks after delivery her blood pressure returned to normal but she remained proteinuric. She ultimatly had a kidney biopsy and was diagnosed with membranous glomerulonephritis. The patient was non-adherent with her treatment and variously treated with cyclosporin, cyclophosphamide and steroids. She aborted a pregnancy at 11 weeks due to cyclosporin exposure. [It is fascinating reading the literature and appreciating the widely varying recommendations and practices regarding the fetal toxicity of renal therapeutics]
The patient was lost to follow-up until she presented at 22 weeks gestation in a third pregnancy with nephrotic syndrome (5g in 24 hours), hypertension and decreasing renal function. The fetus was eutrophic (50% for femur length and biparietal diameter. Explanation).
The patient was started on daily methylprednisolone 16 mg and azathioprine 100 mg. Additionally she was treated with antihypertensives and diuretics. Subsequently the methylprednisolone dose was increased to 32 mg and then to 64 mg/day. Albumin was added to the diuretics. The patient did well until the 29th week when the albumin began to fall. They noted decreased fetal growth rate. In the 33rd week, fetal growth stopped and the patient went for cesarean section. A small for gestational age but otherwise healthy boy was delivered. The boy needed a few days of oxygen and was discharged home after 21 days.
After the patient stopped breast feeding (the article used the term ablactation, new one for me) she started cyclophosphamide and ACEi and went into remission within 3 months. Her subsequent history was marked by multiple relapses and ultimately end-stage renal disease requiring dialysis.
The authors felt this patient was remarkable for the use of a lower dose of steroids, 250 mg methylprednisolone pulses rather than 1g pulses. They felt the lower doses allowed them to avoid some of the side effects of glococorticoids:
  • Intrauterine growth retardation (that’s a stretch since the kid was small for gestational age)
  • Suppression of fetal adrenal glands
  • Periventricular leukomlacia
They attribute the success of the low dose steroids to the use of azathioprine, which is not absolutely contraindicated after the twelfth week.
I am skeptical of the claim that they were able to effectively control symptoms with the lower dose steroids and azathioprine. It looks to me like the patient has progressive worsening of the blood pressure, albumin, proteinuria and renal function. The decrease in the proteinuria may have more to do with the decrease in the GFR than the effectiveness of the therapy.
Malik et al. Repeated pregnancies in patients with primary membranous glomerulonephritis. Nephron (2002) vol. 91 (1) pp. 21-4
Malik presents a retrospective study on patients with MGN with multiple pregnancies with the hypothesis that repeated pregnancies worsen the prognosis of membranous nephropathy and increase the danger of pregnancy. Nine patients and 51 pregnancies were reviewed, 30 of the pregnancies were after the diagnosis of MGN and 21 were before.
All the patients came from a single tertiary care hospital and had their biopsies from May 1985 to December 1997. None of the patients had a renal biopsy during pregnancy.
The first table shows the gross outcomes for the pregnancies:
The data looks pretty promising. One women, patient 6, had terrible pregnancy outcomes:
  1. Fetal loss at 37 weeks associated with pre-eclampsia in the first pregnancy
  2. Spontneous abortion prior to 22 weeks with the second pregnancy
  3. Live-birth complicated by prematurity, pre-eclampsia and cesarean sections. Infant with low birthweight.
  4. Live-birth complicated by prematurity, pre-eclampsia and cesarean sections. Infant with low birthweight.
Outside of patient 6, there was only 1 pre-mature infant with a cesarian section in 26 pregnancies. No fetal deaths and no spontaneous abortions. 
Looking at the progression of renal disease that might have been induced by the pregnancy the data is likewise reassuring. The authors could find no increase in proteinuria or serum creatinine. Only one mother had hypertension and the worst serum Cr was 2.5 mg/dL in patient 5.
The authors conclude:
…the outcome of repeated pregnancies in patients with MGN is good with 90% live births. Repeated pregnancies do not influence the course of MGN.
This report looks great. It never mentions what type of therapy, if any, the patients received. The authors also mentioned that patients with more severe renal disease may have been routed to a different hospital that was a center of excellence in renal disease, suggesting possible selection bias to more mild cases.
References of interest
  1. Abe S et al. The influence of antecedent renal disease on pregnancy Am J Obstet Gynecol 1985; 153: 508-514. 
  2. Jungers Membranous glomerulobephritis and Pregnancy. Clin Nephrol 1988; 29: 106-107
  3. Surian M et al. Glomerular disease in patients with primary and secondary glomerular diseases Nephron 1984; 36:101-105.
Barcelo et al. Successful pregnancy in primary glomerular disease. Kidney Internationsl (1986) vol. 30 (6) pp. 914-9
Barcelo examined 66 pregnancies in 48 women from 1972 to 1981. All of the women had primary glomerular disease. The distribution was:
  • MPGN 16
  • FSGS 13
  • IgA 10
  • MGN 7
  • Focal nephritis 2
The pregancy outcome were generally very good, with MPGN having the worst outcomes. In the 9 pregnancies with membranous nephropathy, 7 were full term, 2 were premature. No fetal deaths.
When looking at proteinuria, the authors found a inverse linear correlation between proteinuria and fetal weight. 
The authors noted an increase in obstetric complications with three risk factors: renal failure, nephrotic syndrome and hypertension:
The incidence of obstetric complications varied with the presence or absence of risk factors. Women with low proteinuria (≤2.5 g/24 hours), without hypertension or renal failure had a low complication rate: 2.8% (one still birth). In the nephrotic syndrome, obstetric complications reached 33% of the pregnancies (pre-term), the same as with moderate renal failure (33% abortion, pre-term) and lower than women with hypertension (62% of the pregnancies, abortion, pre-term).
The authors employed a matched control group to try to assess any progression of renal disease induced by the pregnancy. Like Malik, they were unable to show any damage or worsening of renal prognosis due to the pregnancy. No significant differences between the pregnant and control groups.
The authors concluded that primary glomerular disease was associated with adequate fetal outcomes without damaging the mothers’ prognosis. They speculate that the correlation of proteinuria to birthweight may be due to decreased placental perfusion from intravascular volume depletion from the loss of oncotic pressure.
The authors conclude with a twisted double negative meant to maximally confuse the reader:
The high fetal survival rate and the lack of repercussions of pregnancy on maternal nephropathy in the majority of women reported here indicate that pregnancy in patients with primary glomerulonephritis, glomerulosclerosis without hypertension, or significant renal function impairment should not be advised against. On the other hand, it should be kept in mind that coexistent hypertension worsens the prognosis, and the nephrotic syndrome increases the incidence of pre-term deliveries and low birth weight infants, although fetal viability is not markedly affected.
From the department of “Some docs will try anything” comes this case report of a patient who presents with membranous nephropathy at 9 weeks gestation. She had 21 grams of protein and was started on cyclosporine.  [It is fascinating reading the literature and appreciating the widely varying recommendations and practices regarding the fetal toxicity of renal therapeutics] The patient had an albumin of 1.4. The physicians did a full thrombophilia work-up and found elevated levels of lipoprotein A and fibrinogen. Based on these results they started the patient on prophylactic Lovenox (1.5 mg/kg/d).
At 26 weeks, the patient developed back and flank pain. Ultrasound showed right renal vein thrombosis with extension into the inferior vena cava. The patient was then switched to unfractionated heparin 10 units/kg/hr and a t-PA infusion.
The thrombolytics were working and daily ultrasounds showed progressive reductions in clot volume. On the seventh day, however, the fetal heart rate slowed and the patient went for emergency cesarean section. They stopped the t-PA and heparin in the OR. The baby was born at 720 g, and did well enough to be extubated after 18 days and go home neurologically intact 83 days after birth.
The mother’s course was complicated by 800 mL of blood loss (amazingly little if you think about it), anemia and hypertension but, likewise did well.
I’m trying to draw lessons from this case and the only ones that jump out at me are that heavy proteinuria can cause renal thrombosis in membranous, just like as in non-pregnant patients, and that prophylactic LMW heparin failed, at least in this case. 
Katzir et al. Pregnancy in membranous glomerulonephritis–course, treatment and outcome. Clin Nephrol (2004) vol. 61 (1) pp. 59-62
Katzir presents a case of a 23 y.o. primigravid with previously diagnosed membranous nephropathy stage III/IV, who was admitted at 14 weeks gestation. The patient had initially been diagnosed with membranous at age of 14. She went into complete remission following use of the Ponticelli regimen (true Ponticelli, with alternating chlorambucil and steroids). She had been in remission for more than a year prior to getting pregnant.
Seven weeks into the pregnancy she developed hypertension (160/90) with 1.5 grams of protein on a 24-hour sample. She responded to methyldopa and a low-salt diet (135/70).
At 14 weeks, the patient was readmitted with symptomatic hypertension (160/100). At that time she had 10.6 grams of protein on a 24-hour sample, an albumin of 2.1, and a cholesterol of 324 mg/dL. Renal function remained normal. After informed consent they started IV methylprednisolone 1g a day for 3 days followed by 50 mg a day of prednisone for 4 weeks. This resulted in improved blood pressure, loss of facial edema and a decrease in proteinuria to 6g/day and an increase in albumin to 2.5 g/dL. 
The patient had a second 3 day pulse of 1 gram of methylprednisolone and then oral prednisolone 60 mg every other day. After the second month of therapy, 26th week gestation, the albumin rose to 2.9 g/dL and the proteinuria was down to 4.8 g/24-hours, and the blood pressure was down to 135/80.
At 34 weeks gestation was readmitted with hypertension and uterine cramps. She was induced and delivered by cesarian section. The infant did well and was healthy at 1 year follow-up.
This looks like an effective treatment of membranous nephropathy in pregnancy, in my eyes more compelling than the Sebestyen case report of lower dose steroids and azathioprine. Steroids alone are generally considered ineffective in membranous, hence the use of Ponteceli regimen and tacrolimus as the standard of care. I would describe the steroid pulses as a means to prolong the pregnancy to get the fetus to viability and after delivery allow the mother to seek definitive care.
Packham et al. Membranous glomerulonephritis and pregnancy. Clin Nephrol (1987) vol. 28 (2) pp. 56-64
Packham reviews 33 pregnancies in 24 women with membranous nephropathy.
  • 17 women initially presented during pregnancy
  • 7 women had the diagnosis ante-partum
Of the women who presented during pregnancy 11 of them, received biopsies at the end of the first trimester.
In the 33 pregnancies the outcomes were not as rosy as other studies have shown:
  • 8 pregnancies resulted in fetal death (24%)
    • 6 occurred in the first trimester
    • 3 spontaneous abortions (1 at 14 weeks, 2 in the first 12 weeks)
    • 4 therapeutic abortions
    • 1 still birth at 22 weeks
  • 14 pregnancies resulted in premature infant (32-36 weeks)
    • 60% of pregnancies that went beyond the first trimester had premature delivery
    • 2 babies were born before 32 weeks
  • Two congenital abnormalities
    • hydrocephalus (one of the therapeutic abortions)
    • hare lip
The mother’s outcomes were relatively benign
  • three patients had decrease in renal function
    • 1 lost half of her kidney function, the loss persisted after delivery but remained stable on azathioprine and warfarin. The patient ultimatly stopped those drugs and progressed to ESRD
    • 1 mother had a twin pregnancy and was diagnosed with mild membranous in the first trimester. At 34-weeks she developed ARF, severe hypertension. She was induced and after delivery went for a repeat kidney biopsy which demonstrated crescentic GN. The patient was treated with cyxlophosphamie and had a good outcome with stable renal function.
    • 1 mother had worsening renal function at 14 weeks. Her biopsy revealed fibrinoid crescents. She later spontaneously aborted the fetus. Renal function later normalized.
  • Hypertension occurred in 15 (46%) of the pregnancies.
    • usually in the third trimester
    • resolved after delivery in all but 3 women.
The authors felt that proteinuria was the most important risk factor:
In this, the largest study ever done on membranous nephropathy the authors found, outcomes worse in both the fetus and mothers. This may be attributable to the length of the study. The authors commented that neonatal treatment and anti-hypertensive therapies have gotten much better and this may explain the fact that no child or fetus died after  1975 (the patients were collected from 1964-1986).
Lindheimer and Katz. Gestation in women with kidney disease: prognosis and management. Baillieres Clin Obstet Gynaecol (1994) vol. 8 (2) pp. 387-404.
Lindheimer and Katz. Two of the biggest characters in my fellowship at University of Chicago. Whenever I was with them they would trade stories that left them both in stitches and mostly bewildered me. Adrian Katz was my mentor in clinic for my first year of fellowship and his last year of clinical medicine. It was an interesting pairing.
This is a book chapter masquerading as a journal article. It’s huge. The chapter leads off with three conclusions the authors derived from reviewing 9 articles covering over 1,000 pregnancies:
  1. women with renal disease but ony mild decreases in renal function and normal blood pressure at conception will do well and the pregnancy does not adversly affect their renal prognosis. They specifically exclude lupus, MPGN, scleroderma and pariarteritis from this conclusion.
  2. If the patient has a creatinine ≥1.5 and >3 mg/dl or hypertension at conception about a third of patients will lose further renal function during pregnancy and have further loss of function post-partum.
  3. Women with a creatinine ≥3 mg/dl are frequently infertile and when they do conceive the liklihood of a successful outcome is low with high maternal morbidity.
The remainder of the chapter/article goes on to provide data to support the above conclusions. They lead off reviewing Katz’s own article from 1980 covering 121 pregnancies with intact renal function (Cr ≤ 1.4) and normal blood pressure (ony 20% had hypertension). The series excluded lupus nephritis. The outcomes are summarized below and have excellent outcomes:
The graph on the left is pregnancy outcome, on the right is the long-term follow-up for the mothers.
Ptoteinuria was common and was often nehrotic range. Katz found that the prpteinuria was usually well tolerated and did not influence the pregnancy outcome.
  • 121 pregnancies
  • 5 still births
  • 6 neonatal deaths
  • 91% success rate
Impressive, especially considering that most of these deliveries were in the 60’s and 70’s. He quotes a study by Abe, with more contemporary neonatal care that noted no perinatal deaths in mothers with IgA despite 20% preterm deliveries. 76% of the infants were of adequate size for gestational age, so renal disease does not necessarily result in small babies.
The 5 patients that ended up oin ESRD did so 2-8 years after the pregnancy and their diagnosis was a rogues gallery of renal badness: amyloidosis, FSGS, ADPKD, and 2 cases of crescentic GN.
Then this table. Wow that is awesome:
This table summarizes the 6 studies published after Katz’s 1980 article and generally support Katz’s initial conclusion that as long as the renal function is pretty good and the blood pressure is okay going into pregnancy the outcomes are acceptable.
The article looks at the data on IgA nephropathy, where there is some controversy. A number of authors (Kincaid-Smith,  Becker GJPackham 1234) have reported worsening of proteinuria, blood pressure and renal function during pregnancy. This was associated with fetal loss in 27% and on biopsy, woman who had a history of pregnancy tended to have more severe lesions. Other studies have shown beter outcomes with IgA and a lack of adverse outcomes compared to their nulliparous peers:
So Katz and Lindheimer conclude that for IgA:
Thus the observations of most investigators is that women with IgA nephropathy who are normotensive and have preserved renal function should anticipate few problems and that there is no convincing evidence linking gestation to progression of their disease.
The authors then describe some conflicting data on FSGS but generally reinforce their initial conclusions that patients with intact renal function be counseled that pregnancy is generally safe and a good outcome should be expected.
Lupus is a condition where, if the disease has been active in the 6 months prior to pregnancy, the prognosis is more guarded. They also mention a progressive post-partum renal failure due to thrombotic lesions in patients with anti-phospholipid antibody syndrome.
The authors feel that woman with scleroderma or periarteritis should be counseled against pregnancy and go as far as suggesting therapeutic abortions if the condition is present in the first trimester. Successful pregnancies with scleroderma have been managed with ACEi, a drug considered to be teratogenic.
The chapter then discusses women with more severe renal disease going into pregnancy. Bear and Kincaid-Smith (unable to find the ref) both reported permanent and severe losses of renal function associated with pregnancy in roughly haf the pregnancies. More contemporary studies have largely supported the worse outcomes with typically a quarter of patients suffering acceleration of renal disease. 85% of pregnancies were successful.
The next section is on nephrotic syndrome. The authors oint out that albumin physiologically falls 0.5-1.0 g/dL in pregnancy, so patient with proteinuria may slip into nephrotic syndrome as the serum albumin falls further. This is called cyclic nephrotic syndrome of pregnancy. Though there is some disent in the literature, the consensus is that nephrotic syndrome alone does not result in poor outcomes.
Kand L then examine the renal biopsy. They recounted the 1965 paper “Bleeding after renal biopsy in Pregnancy” which described poor outcomes after 77 renal biopsies in pregnancy:
  • 16.7% gross hematuria
  • 4.4% perirenal hematomas
  • one maternal death
Kand L discuss their own reviews of the literature which found major biopsy complications occur during transperitoneal renal biopsies done during c-sections, biopsies with uncorrected coagulation abnormalities and biopsies with uncontrolled hypertension. They thern reported the excellent results at Chicago Lying-in Hospital with 3.5% hematuria following 400 biopsies.
In 1987 Packham and Fairley reported on 111 biopsies with a hematuria rate of only 0.9%.
They conclude that biopsey is safe in pregnancy.
They recommended biopsy in the following situation:
  • sudden deterioration of renal function before 32 weeks
  • symptomatic nephrotic syndrome before 32 weeks
They woud defere biopsy when there is
  • proteinuria alone, with normal blood pressure and normal renal function.
  • hematuria alone, with normal blood pressure and normal renal function.
They argue that active sediment (red and or white cell casts) is a relative indication for biopsy as a diagnosis of scleroderma would prompt termination of the pregnancy.
  • basic metabolic profile
  • BUN
  • albumin
  • fasting lipid profile
  • 24-hour urine for:
    • creatinine
    • protein
  • uric acid
  • PT, PTT, INR
  • CBC d/p
The patient should be followed every 2 weeks until week 32 and weekly after that. Renal parameters should be checked at least every month.

In defense of the epigraph

I was listening to the Slate Cultural Gabfest on my way to work this morning and Julia Turner asked the audience to defend the epigraph, the quotations that some authors use to lead off a book or chapter.

The Fluid and Electrolyte Companion used an epigraph that I thought was perfect and communicated the mood I wanted readers in as they read the book:

The quotation is from Dr. Strangelove and General Ripper (the man with the cigar) says it in the scene captured in the picture at the top of If you haven’t seen the movie you really should. It is one of Stanely Kubrick’s masterpieces and possibly the funniest movies I have ever seen.

What touched me was how similar I am to General Ripper. Here was a man who spent all of his time thinking about precious bodily fluids and every time he captured someone in his vacinity and started to explain how wonderful and important they are, the other person just got nervous, uncomfortable and wanted to squirm away. In the header picture, imagine me as General Ripper talking about pseudohyponatremia and imagine Group Captain Mandrake being played by an unsuspecting innocent medical student who is randomized to one of my medicine teams.

The mood I wanted to establish was that this text book was lighter than Guyton’s physiology, we would poke fun at medicine and you could unbutton the white coat and relax a little while reading this text. I think the epigraph absolutely nailed this mood.

By the way if you downloaded the book before this week, re-download it. I just added the leading 10 pages which include the introduction, dedication, colophon, table of contents and epigrpah.