Last night I went to a dinner with a distinguished speaker, an emeritus professor, who began by talking about past mentors in his field. One of these leaders is memorialized by a statue of him at a chalkboard because he was such an “amazing teacher.” The floor of the statue around him is littered with dimes.
Why? Because when a student, resident, or other trainee answered a question wrong, he would hand them a dime and tell them to call their mother because she was the only one who would love them now.
What an asshole! Instead of being a real teacher who allows trainees to make mistakes and learn from them, he humiliated them in public. And someone felt a statue to lionize this behavior was in order?
Too many of academic medicine’s “elder statesmen” laud the “tough love” of the good old days. Just because some of us survived and thrived under such conditions does not mean they were good for us. I wonder about learners who looked to other fields of work because they were too stupid to follow in this “great man’s footsteps.”
Teachers should have respect for their learners. Public denigration is never the answer. You can correct an answer without humiliation.
Back in 1987, the year I gave birth to my firstborn, Diane Keaton starred in Baby Boom, my first recollection of the Frenzied Female archetype. Her character, a driven yuppie known as the Tiger Lady, inherits a girl from distant relatives. This hyper successful businesswoman proves incapable of hiring a competent nanny. Ultimately, she ends up moving to a farm in the country. After hilarious escapades, she starts a successful business and falls in love with the local veterinarian and her “less complicated” life with child.
Yeah, right. Now I must admit children do strange things to you and your ambitions. Priorities can get reordered in a hurry when that bundle of joy (and excrement) lands in your arms. However, no one’s level of competence should be as compromised as the character Keaton portrayed.
There are other examples. In 2002 Allison Pearson brought us the life and times of a British hedge fund manager, Kate Reddy, who also seemed unable to hire adequate help with two young children at home. Of course, the opening scene of Kate “distressing” store-bought pies to make them seem homemade was hysterical. Her professional life remains more intact than the boss in Baby Boom, but she still seems to be one misstep away from getting sacked all the time. Really? A woman who can manage that many currencies across multiple time zones can’t keep her calendar in check? Of course, she does make a career change by the end of the story. We wouldn’t want her to succeed at all aspects of her life, would we?
I just finished a nice debut novel, The Queen of Hearts, by Kimmery Martin. This time the Frenzied Female is Zadie, a pediatric cardiologist who has managed to not only become a pediatric sub-specialist but also has 4 children with her investment banker husband. Her life seems to always be on the edge of chaos, with a delicate time balance of carpools and events, yet she always has time to drop everything for her BFF from college and medical school. Her spouse is constantly jetting off to some foreign meeting, leaving her to juggle their home life. Once again, they have not hired adequate help for the lives they live. I have some bones to pick with some of the medical stuff in the novel, but in general, it was a fun read that kept my tablet in my hand. It was also nice that Zadie’s career does not suffer through the novel as in the earlier examples.
I’m frustrated that we see the same Frenzied Female. In 30 years, we still laugh at that poor woman who hasn’t figured out that she cannot manage it all.
Over the years, the Manic Pixie Dream Girl has become a common trope in books and media, despite no evidence that such creatures exist. Most MPDGs arise from the male imagination, while women writers were involved in all of the FFP examples above. There is a bit more truth to this archetype, but I do wish it would evolve. Could we admit that we have someone (looking at you Amazon) deliver stuff to our home, rather than making grocery runs all the time? Or hired a nanny who can actually do the job of hauling children around town?
The life of the FFP can be chaotic, madcap, and funny, but women do not lose their ability to organize and function while they raise children. All of these are women with money and resources, those best able to take on the child raising role. If we can’t picture these educated, well-paid women doing these tasks, what hope do working-class families have?
We have all had that self-doubt at times, wondering if we were really qualified to do what we do. In some people it becomes debilitating, preventing them from pursuing opportunities.
Most of us suck it up and struggle through the self-doubt, usually with some version of “fake it till you make it.”
I heard a new approach yesterday in an interview with Todd Herman, an internationally recognized coach. He suggests having an alter-ego who has qualities that you lack. For example, he is often indecisive, but his business alter-ego has no such problem. He assumes his other identity by putting on glasses (which he does not need).
This reminds me of when my daughter had to do unpleasant tasks, like cold-calling for donations for fundraisers. She has a theater background, and she became “Fundraiser Jenny.” People weren’t rejecting Jen; they were saying no to the other character.
I’m going to try this for some upcoming situations and see how it works. How about it? Do you ever assume a secret identity?
An Illinois Public Radio story caught my eye on Twitter this week. It dealt with a major player in Chicago charter schools and their disciplinary policies. Limitations on bathroom usage meant many young women were bleeding through the mandatory khaki pants during their periods, a less than ideal situation for all involved:
“We have (bathroom) escorts, and they rarely come so we end up walking out (of class) and that gets us in trouble,” she texted. “But who wants to walk around knowing there’s blood on them? It can still stain the seats. They just need to be more understanding.”
They go on to defend the policy, noting that girls who bleed through their pants can tie a sweater around their waist to cover up the damage. Of course, since this is not a usually acceptable part of the dress code, they then announce the names of the girls who are allowed to wear this aberration.
Yeah, please announce to the world the name of the menstruating students. Nothing about that will make them feel self-conscious or awkward.
I haven’t worried about bleeding through for a while now, but I do worry about bathroom access in schools. As a pediatric nephrologist, I take care of a lot of children who would benefit from easier access to the restroom.
First up are those children with frequent urinary tract infections (UTIs). One of our defenses against UTI is completely emptying our bladders on a regular basis. This action flushes out any bacteria that have made their way into the interior space. In addition to that, holding urine can cause the bladder to lose efficient function. Children may not be able to empty completely, meaning bacteria are more likely to get a foothold in the bladder and cause trouble.
Second, we must consider children with constipation. A large wad of poop can put pressure on the bladder, its outlet, and its nerves, preventing proper sensation and function. These children must be cleaned out with aggressive stool softening. How inconvenient if the bathroom escort is not available when the poop is ready to pop! Holding it in not only makes constipation worse but further worsens bladder function and makes UTI likely. Adequate fluid intake can also prevent constipation.
Third, a lot of children get kidney stones. Some of these kids have biochemical problems that can be treated, but even those stone-formers could likely prevent such things if they drank enough water. For adults, we recommend enough water to produce 2 liters (66 oz) of urine daily. This means drinking 2-2.5 liters of fluid. At least part of this should be consumed during the school day, necessitating bathroom use. Kidney stones produce debilitating pain, and in the long-run can lead to permanent kidney damage.
Other considerations include keeping bathrooms clean and functional and safe.
I would like to declare that all people, even students, have the right to use the bathroom when necessary. Not only is holding pee and poop in harmful, but I cannot imagine being able to learn when I’m worried about losing control or bleeding through my clothing.
Join me in showing support for the right to hygienic elimination! You can buy a “Let Kids Pee” ceramic cup or stainless steel travel mug on Amazon (my design is featured above in this post). You will help support this website and the battle we pediatric nephrologists fight on this front.
This year a number of abstracts about sickle cell and the kidney caught my attention, having just initiated dialysis on a patient with HbSS. Since the science forces of the universe seemed determined to focus my attention on this disorder, I gave into their wishes.
Hemoglobin (hb), the molecule that carries oxygen to tissues in our body, is composed of two alpha protein chains and two beta chains. In the HbS mutation, a single change in the beta chain changes the structure of the protein so that when oxygen levels drop, it becomes straighter instead of round, stretching red blood cells into a crescent or sickle shape. Abnormally shaped red blood cells are prone to damage (hemolysis) and may clog the smallest vessels in the body, resulting in organ damage and pain.
If a child gets one copy of the HbS gene, then they are a carrier; this condition is also called sickle cell trait and occurs in 1 in 13 African American babies. Most people with trait have no symptoms, although under conditions of low oxygen their disorder may be unmasked. For example, the central part of the kidney (the medulla) has much lower oxygen tension normally. Cells often sickle there and cause damage, so individuals with otherwise asymptomatic sickle trait may not be able to fully concentrate their urine.
If a child gets a copy of HbS from both parents, then they have HbSS, the full-blown sickle cell anemia disease. This happens to about 1 in 365 African American children. These individuals have anemia because the sickling cells don’t last as long as those with normal Hb (3 weeks vs 3 months). The abnormally shaped cells may also impair blood flow to organs cause acute pain episodes, what most people think about with sickle cell disease. In addition, other organs may be damaged by these events, including the brain, heart, lungs, and kidneys.
The first poster on my list dealt with KIM-1 (Kidney Injury Molecule 1) as a new biomarker for kidney damage in a humanized mouse model.They followed glomerular filtration rate (GFR) and urinary biomarkers in HbSS mice and genetic controls every 4 weeks for 24 weeks starting at 8 weeks of age. At that starting point, no differences in GFR or proteinuria were demonstrated. By 12 weeks, the HbSS mice had a significant rise in GFR and proteinuria. By 32 weeks of age, GFR was lower in HbSS than Hb AA mice, even as proteinuria climbed higher. Urine biomarkers demonstrated early KIM-1 as a potential predictor of loss of GFR later in the course. Not included in the abstract was a cohort of patients with HbSS, some of whom have developed elevated KIM-1 excretion. This has the potential to drive important translational studies in the future.
The next poster looked at renal cilia in this same mouse model. Ciliary disorders often result in cysts in the kidneys, and patients with HbSS have an increased risk of cyst formation. Kidneys from HbSS mice have reduced ciliary proteins in their kidneys, suggesting reduced numbers or size of cilia in this model. Additional studies applied hypoxic stress to the mice, a maneuver that increased expression of the proteins under study. These experiments are still preliminary, but I would never have guessed that cilia would be a problem in sickle cell kidneys.
The final poster examined the role of Hb uptake in tubular cells in nickels cell disease. Much of this study occurred in vitro, examining what happened to tubular transport when free Hb gets filtered and the tubules reabsorb it. It competes for transport with a number of other proteins, such as albumin and the vitamin D binding protein. Patients with HbSS have reduced red blood cell lifespan and episodic hemolysis, so they do filter higher amounts of free Hb. They also seem to be much harder to make replete with Vitamin D. These basic science observations may help explain some interesting clinical observations, even though these phenomena would seem unrelated at first glance.
Sometimes an abstract just grabs me; this time, three of them jumped me and made me write about them. All were really good science with excellent presenters, and a lot more information than I’ve included here (click the links, people). Best of luck helping us understand this difficult consequence of a fairly common disorder.
Each kidney contains a bunch of discrete units or nephrons that include a filtering unit, the glomerulus, and a tubule that reclaims all the useful stuff from the filtrate. When we discuss how the kidneys work, we often treat the kidney like it’s a single nephron, but it’s a whole bunch of units that need to be on the same page regarding the body’s requirements.
Postnov D, Marsh DJ, Holstein-Rathlou N-H, Cupples W, and Sosnovtseva O: High-resolution optical imaging of synchronization in the renal circulation.
I have a difficult time doing this poster justice, since I do not have images to post. Suffice it to say that they have a laser speckle imaging set up that provides spatial resolution to 0.8 μm per pixel. They were able to analyze clustering of flow in ~1.5 x 1.5 mm^2 areas of renal cortex and gauge how well synchronized flow was.
This is a cool toy I would love to play with, and I can imagine some interesting studies coming from this new technology. If you missed the poster, check out the abstract above.
Glucose in the glomerular filtrate gets reabsorbed in the proximal tubule by two transporters, known as sodium-glucose cotransporters (SGLT). The bulk of the glucose gets removed by SGLT2 with a smaller amount retrieved farther down the tubule by SGLT1. With normal blood sugar levels, these molecules can reclaim all the filtered load of glucose, leaving none of this sugar in the urine.
In diabetes, glycosuria occurs when blood sugars exceed the limits of SGLTs. Agents have been around for a while that inhibit these transporters, but only recently have inhibitors of SGLT2 been shown to reduce blood glucose in diabetes in clinical settings. Large trials over the past couple of years have shown additional benefits of this class of drug beyond their ability to reduce hyperglycemia. They seem to reduce cardiovascular events and to have beneficial effects on progression of diabetic kidney disease.
Liu Z, Hall E, and Singh P: SGLT2 inhibition decreases oxygen consumption and increases oxygen tension in diabetic rats
Sodium reabsorption drives metabolic demand for oxygen consumption in the kidney. In addition to allowing glucose to escape, SGLT inhibitors prevent sodium reclamation and reduce this demand. They found that diabetes increased renal oxygen consumption as previously demonstrated and the SGLT inhibitor Empagliflozin (EMPA in figure) prevented this change. Oxygen tension in the renal cortex was reduced by diabetes, with SGLT inhibition once again preventing this change. Medullary oxygen tension was not affected by these states.
SGLT inhibitors may have important effects in organs aside from lowering blood glucose. Studies like these may help us understand these interesting new agents, and point toward other therapeutic targets.
On Sunday David Mattson presented the Starling Distinguished Lecture of the American Physiological Society Water and Electrolyte Homeostasis Section. His talk addressed the role of inflammation in salt-sensitive hypertension, using the Dahl salt-sensitive rat and some supporting human data.
About half of human adults have hypertension, and about half of those patients are salt-sensitive like this rat. Feeding this rodent a high salt diet leads to rising blood pressure and albuminuria, with enlarged glomeruli, tubular damage, and inflammation. Other types of rats given the same level of sodium intake do not develop these findings. Studies from people with hypertension also show increased lymphocytes in their kidneys, suggesting that there are parallels with human disease.
In a series of experiments, Dr. Mattson showed that there were increased B and T cells in these rat kidneys and that the immune cells were activated and producing a number of cytokines. Inhibiting the presence and activity of these immune cells attenuated both the hypertensive and renal damages induced by salt loading. They then took genes identified in human association studies of hypertension and mutated the analogous genes in rats. They transplanted bone marrow from these mutant animals into Dahl rats without the mutation, so only hematopoietic cells carried the mutation in question. When salt loaded, these rats showed less hypertension than intact Dahl rats, suggesting that the immune response provided major input for hypertension.
What about the role of hypertension beating up on these kidneys? Dahl rats have poor autoregulation, so systemic hypertension gets transmitted to the kidneys. They placed an aortic cuff just above the left renal artery in rats and used it to maintain a normal blood pressure into that kidney. The right kidney saw and felt the higher pressure. This maneuver alleviated the inflammatory response in the cuffed kidney.
In the Dahl model of salt-sensitive hypertension, both inflammation and barotrauma appear to contribute to kidney damage. The story does not end here; the Mattson lab is presenting more fascinating work on this topic at this year’s meeting.
This year the Renal Section Young Investigator Award goes to a favorite of mine, and not just because her work has let me create a great image of the kidney. Jennifer Pluznick, now an Associate Professor at Johns Hopkins, began her journey in physiology as a doctoral student at University of Nebraska while I was there. While a post-doctoral fellow at Yale, she began exploring G-protein-coupled-receptors (GCPRs) in the kidney, especially those previously involved with smell, and her lab now explores their role in kidney function. Her lab logo is pretty cool; I’ll wait while you take a look.
Olfactory receptors constitute the largest gene family with 350 members in humans and approximately 1000 members in rodents. So far, 18 of these olfactory receptors have been located in the kidney with an additional 11 taste-associated GCPRs and 76 without known ligands. She first studied olfactory receptor 78 (Olfr78), an interesting chemosensor that localizes to the afferent arteriole, a major site of control for blood pressure and kidney function. It’s ligands (activators) include short-chain fatty acids such as acetate and proprionate, molecules derived primarily from our gut microbiota. Proprionate has been shown to cause the release of renin via its interactions with Olfr78.
Changes in gut microbiota have been associated with changes in blood pressure, so her lab wanted to explore changes in the metabolites that might occur with hypertension. They implanted micro pumps into conventional mice and into germ-free mice (mice in a plastic bubble) and infused them with angiotensin II, an established model of hypertension. Germ-free mice showed no changes (no microbiome, no metabolites), but of more than 800 substances studied, 13 were unregulated with angiotensin II infusion. Some are uremic toxins and many are known to lower blood pressure; perhaps our microbiome is trying to help us out when our kidneys fail or our blood pressures otherwise get elevated. After all, our death would not be particularly helpful for the bacteria residing in our gut. Also interesting were some sex-specific changes identified. The meaning of these differences should provide fertile ground for further study.
As expected, Dr. Pluznick delivered an excellent presentation of her impressive work. If you aren’t here, you missed a great talk. You can still catch her on the TED stage: