A chapter by chapter recap of Burton Rose’s classic, The Clinical Physiology of Acid Base and Electrolyte Disorders, a kidney physiology book for nephrologists, fellows, residents and medical students.
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Lety referenced the Cr x 20 formula, a strategy to multiply the serum creatinine by 20 to estimate the initial furosemide dose. We agreed that this is more appropriate than the House of God formula of age + BUN = dose (which may be so much higher).
JC”s abstract on use of loop diuretics in hepatorenal syndrome type 1 was ultimately published in the American Journal of the Medical Sciences: https://doi.org/10.1016/S0002-9629(23)00623-7
- Presence of counterbalancing antinatriuretic forces
- Ang2
- Aldo
- Low systemic BP
- Adds rate of drug excretion as # 2 and a half
- Almost all diuretics are protein bound
- So not well filtered
- Enter tubule through organic anion and organic cation transporter
- This can limit diuretic effectiveness
- Natriuretic response plateaus at higher rates of diuretic excretion due to complete inhibition of the diuretic target
- This plateau in normal people is 1 mg of bumetanide and 40 mg of furosemide given IV
- Double this for oral furosemide, no adjustment needed for bumetanide
- 15-6
- Refractory edema
- Start with a loop diuretic
- Initial aim is to find the effective single dose
- From the paragraph this is about threshold dosing
- Double ineffective doses until good effect
- Suggests maximum furosemide dose is 200 mg IV and 400 mg oral
- Excess sodium intake
- High sodium diet can work to prevent patients from achieving negative sodium balance.
- Suggests diets after leaving the hospital maybe higher in sodium
- Decreased or delayed intestinal absorption
- Decreased intestinal perfusion, reduced intestinal motility and mucosal edema may contribute.
- But why is this worse with furosemide than with bumetidine or torsemide?
- Decreased drug entry into the tubular lumen
- Thiazides don’t work below a GFR of 20
- CLICK
- Renal failure
- Increased organic anions compete for diuretic secretion
- Bumetidine isn’t as dependent as furosemide on GFR
- Use 1/20th rather than 1/40th the dose
- Maximum of 8 to 10 mg
- Furosemide has ototoxicirty at high doses, he advises against 2400 mg/day
- There is a Na-K-2Cl carrier in the endolymph producing cells
- Ethacrynic acid has the most ototoxicity
- Only loop or thiazide that isn’t a sulfonamide derivative
- Cirrhosis
- Spiro is diuretic of choice
- More effective than loops alone
- Does not induce hypokalemia that can cause hepatic encephalopathy
- Cirrhosis causes marked hyperaldo
- Loop diuretics have to compete with bile salts for secretion in the proximal tubule
- Spiro does not need to be secreted in the proximal tubule
- Recommends to 100 to 40 spiro to furosemide ratio
- And can double this to 200 and 80/day
- and a maximum of of 400/160
- Hypoalbuminemia
- <2 g/dL associated with decreased diuretic entry into the lumen
- Protein binding keeps diuretics in the blood, reduces the volume of distribution
- This maximizes the delivery to the kidney
- In nephrotic syndrome tubular albumin can bind diuretic and prevent its activity
- Co administration of albumin with diuretic has resulted in modest improvements in diuretic effectiveness in various studies
- Intravenous infusion of loop diuretics
- Infusions are greater than bolus
- But if patient is not responding to blouses unlikely to respond to infusions since bolus provides a temporary spike in plasma level
- Increased distal reabsorption
- Increased distal sodium reabsorption decreases the effectiveness of proximal diuretics
- Due to aldo and increased sodium delivery
- Mentions that thiazides have a proximal effect (is that inhibition of carbonic anhydrase?)
- 15-8 is very cool
- Says all thiazides are created equal
- Article from 1972 is why people use metolazone in advanced renal disease
- When doing sequential nephron blocked be careful
- Loss of lots of fluid
- Loss of lots of potassium
- Loss of 5 liters and 200 mEq of K a day is possible with sequential nephron blockade
- Decreased loop sodium delivery
- With heart failure and cirrhosis increased proximal resorption mediated by Ang II markedly reduces delivery of fluid to the diuretic sensitive sites.
- Acetazolamide makes sense here
- Supine or 10 degree head down can increase cardiac output possibly increased venous return
- Can double Na excretion
- Increase CrCl 40%
- CAVH enters the chat!
- Other uses of diuretics
- Met alk, RTA, DI, hyponatremia due to SIADH, hypokalemia
- Diuretics and prostaglandins
- Loops and thiazides increase renal generation of prostaglandins
- Can cause venous dilation may help with acute pulmonary edema
- Can help without increased diuresis
- NSAIDS counter the effect of loop diuretics
- Is this natriuretic effect of PGE? Or due to renal ischemia due to unopposed Ang2 and norepi
- They also raise BP and reduce cardiac output due to increased vascular resistance
- Vasoconstrictor effect of loop diuretics
- One hour after loop diuretics increase vasoconstriction and rise in systemic blood pressure
- Increased Renin and norepinephrine, resolved 4 hours later
- Seen in heart failure and cirrhosis
- In cirrhosis decrease in RPF and GFR of 30-40% with furosemide
Chapter Fifteen: Clinical Use of Diuretics, part 1
Saison 1 · Épisode 21
lundi 13 mai 2024 • Durée 02:00:56
Outline Chapter 15 — Clinical Use of Diuretics
- Among most commonly used drugs
- Block NaCl reabsorption at different sites along the nephron
- The ability to induce negative balance has made them useful in multiple diseases
- Edematous states
- Hypertension
- Mechanism of action
- Three major classes
- Loop
- NaK2Cl
- Up to 25% of filtered sodium excreted
- Thiazide
- NCC
- Up to 3-5% of filtered sodium excreted
- Potassium sparing
- ENaC
- Up to 1-2% of filtered sodium excreted
- Each segment has a unique sodium channel to allow tubular sodium to flow down a concentration gradient into the cell
- Table 15-1 is interesting
- Most of the sodium 55-655 is reabsorbed in the proximal tubule
- Proximal diuretics would be highly effective if it wasn’t for the loop and other distal sites of Na absorption
- Loop Diuretics
- Furosemide
- Bumetanide
- Torsemide
- Ethacrynic acid
- NaK2Cl activated when all four sites are occupied
- Loop diuretic fits into the chloride slot
- In addition to blocking Na reabsorption results in parallel decrease in calcium resorption
Melanie was enchanted by work from RA McCance who did early experiments to induce sodium deficiency using very low sodium diets and a homemade sauna-like tent. His musings are fascinating. Lancet 1936 Experimental human salt deficiency MEDICAL PROBLEMS IN MINERAL METABOLISM
Chapter Eight: Regulation of The Effective Circulating Volume
Saison 1 · Épisode 10
vendredi 26 août 2022 • Durée 01:41:01
References for chapter 8
Robert Schrier proposed a unifying hypothesis to explain the sodium retention seen in edematous states like cirrhosis and heart failure, coining the term effective arterial blood volume (EABV). An open access review in JASN 2007 can be found here: https://jasn.asnjournals.org/content/18/7/2028#ref-3
Epstein FH et al. Studies of the antidiuresis of quiet standing: the importance of changes in plasma volume and glomerular filtration. JCI 1950. In this classic report, investigators studied their own sodium excretion supine, standing and with a variety of maneuvers (saline or albumin infusion) and showed that urinary sodium excretion is limited in the upright position compared to supine position. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC436228/pdf/jcinvest00414-0077.pdf
An interesting review of early concepts on hypertension feature notes on John J Hay and Paul Dudley White. The former was known to say, “The greatest danger to a man with high blood pressure lies in its discovery because then some fool is certain to try and reduce it!” and the latter has been quoted as saying that hypertension might be compensatory but apparently, these quotes are out of context. To find out what they really said, check out: Elias MF and Goodell AL. Setting the record straight for two heroes in hypertension John J Hay and Paul Dudley White. J Clin Hypertens 2019
Chapter Seven: The Total Body Water and The Plasma Sodium Concentration
In this invited piece, Sands and colleagues explain that although urea is permeable across membranes, this is slow, thus urea transporters in the kidney, under control of vasopressin, are needed to facilitate transport and create the medullary gradient.
ADH appears to have an effect on potassium excretion. This was investigated by Giebesch who found, with clearance and micropuncture studies in rats plus isolated perfused tubules, ADH increased potassium secretion A corollary should be that inhibition of ADH would increase the risk of hyperkalemia but this was not observed in the SALT-1 and SALT-2 trials. 5% of patients developed hyperkalemia in both the tolvaptan group and the placebo group
I believe this is the original study looking at urine sodium and blood pressure in the Yanomamo Indians, but the INTERSALT trial linked above I believe had more robust urine data
This study mentions the average lipid profile for men and women along with BMI.
Chapter Four: The Loop of Henle and Counter Current Exchange
Saison 1 · Épisode 5
mercredi 23 juin 2021 • Durée 01:44:08
Show notes with a full set of references are available here: http://www.rosebook.club/episodes/2021/6/22/chapter-four
Also, please fill out our listener survey: https://forms.gle/DVdcJikKZkzY56mXA
Chapter Three: The Proximal Tubule
Saison 1 · Épisode 4
lundi 10 mai 2021 • Durée 01:21:38
Chapter Three: How the proximal tubule is like Elizabeth Warren and other
truths my friends from Boston taught me
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- Increase in stones and nephro albinos is especially premature infants which can increase calcium excretion 10-fold
- Thiazide
- Even though they are less potent than loops they are great for hypertension
- “Not a problem in uncomplicated hypertension where marked fluid loss is neither necessary nor desirable”
- Some chlorothiazide and metolazone also inhibit carbonic anhydrase in the proximal tubule
- Increase Calcium absorption. Mentions that potassium sparing diuretics do this also
- Potassium sparing diuretics
- Amiloride
- Spironolactone
- Triamterene
- Act at principal cells in the cortical collecting tubule,
- Block aldosterone sensitive Na channels.
- Discusses the difference between amiloride and triamterene and spiro
- Mentions that trimethoprim can have a similar effect
- Spiro is surprisingly effective in cirrhosis and ascites
- Talks about amiloride helping in lithium toxicity
- Partially reverse and prevent NDI from lithium
- Trial Terence as nephrotoxin?
- Causes crystaluria and casts
- These crystals are pH independent
- Faintly radio opaque
- Acetazolamide
- Blocks carbonic anhydrase
- Causes both NaCl and NaHCO3 loss
- Modest diuresis de to distal sodium reclamation
- Mannitol
- Nonreabsorbable polysaccharide
- Acts mostly in proximal tubule and Loop of Henle
- Causes water diuresis
- Was used to prevent ATN
- Can cause hyperosmolality directly and through the increased water loss
- This hyperosmolality will be associated with osmotic movement of water from cells resulting in hyponatremia, like in hyperglycemia.
- Docs must treat the hyperosmolality not the hyponatremia
- Time course of Diuresis
- Efficacy of a diuretic related to
- Site of action
- Dietary sodium action
- 15-1 shows patient with good short diuretic response but other times of low urine Na resulting in no 24 hour net sodium excretion.
- Low sodium diets work with diuretics to minimize degree of sodium retension while diuretic not working
- Also minimizes potassium losses
- Increase frequency
- Increase dose
- What causes compensatory anti-diuresis
- Activation of RAAS and SNS
- ANG II, aldo, norepi all promote Na reabsorption
- But even when prazosin to block alpha sympathetic and capto[pril to block RAAS sodium retention occurs
- Decrease in BP retains sodium with reverse pressure natriuresis
- Even with effective diuresis there is reestablishment of a new steady state
- Diuresis is countered by
- Increases in tubular reabsorption at non-diuretic sensitive sites (neurohormonal mediated)
- Flow mediated in creases in Tubular reabsorption distal to the diuretic from increased sodium delivery.
- Hypertrophy
- Increased Na-K-ATPase activity
- Decreased tubular secretion of diuretic if renal perfusion is impaired
- Getting to steady state requires
- Diuretic dose and sodium intake be constant
- Sodium balance is reestablished with 3 days of a fixed diuretic dose
- K balance in 6-9 days
- Figure 15-2
- Which means that people on stable doses of diuretics don’t need regular labs, the abnormalities will emerge quickly.
- Maximum diuresis happens with first dose
- Figure 15-3
- Fluid and Electrolyte complications
- Volume depletion
- “Effective circulating volume depletion also can develop in patients who remain edematous. Although fluid persists, there may be a sufficient reduction in intracranial filling pressures and cardiac output to produce a clinically important reduction in tissue perfusion.”
- Azotemia
- Decreased effective circulating volume with diuretic therapy also can diminish renal perfusion and secondarily the GFR.
- Describes the traditional reason for increased BUN:Cr ratio
- Then states that as much as a third of of the rise in BUN may reflect increased urea production; it is possible, for example, that reduced skeletal muscle perfusion leads to enhanced local proteolysis. This increases urea production.
- Hypokalemia
- Loop and thiazide increase urinary potassium losses
- Often lead to hypokalemia
- 50 mg of HCTZ drop K by 0.4 to 0.6 mEq/L with 15% falling below 3.5
- He uses “associated” I think this is a place where we can use cause
- 50 mg of chlorthalidone
- K falls 0.8 to 0.9 mEq/L
- Etiology
- Increased distal delivery of Na and water
- Increased aldo
- From volume depletion
- Underlying disease: cirrhosis and heart failure
- Talk a lot about significance.
- Info sounds dated
- Increased risk of SCD in MRFIT trial
- Association with increased ventricular arrhythmia with hypokalmia
- Increased PVC and complex PVC by 27% with each drop in K of 0.5 mEq/L
- Says that stress can induce epinephrine which can shift potassium inside cells leading to fatal arrhythmia especially if the patient begins at a low potassium concentration
- Says v-fib two fold likely in MI patients with hypokalemia
- Talks about crazy doses of HCTZ and Chlorthalidone 50+mg
- Recommends 12.5 to 15 mg respectively
- Metabolic alkalosis
- Caused by loop and thiazide diuretics
- Two factors cause this
- Increased urinary H loss
- Partly UE to secondary hyperaldo
- Contraction of extracellular volume around remaining bicarb
- Why not contraction hypernatremia, contraction hyperkalemia, etc?
- Aldosterone contributes by stimulate ing H-ATPase
- Loop diuretics can also stimulate net H loss by increased Hsecretion in the cortical aspect of the thick limb
- This segment has two luminal entry points for na, the traditional NaK2Cl and Na-H exchanger
- Blocking NaK2Cl with loop diuretic stimulates the Na-H exchanger
- Can use NaCl or acetazolamide to treat
- Metabolic acidosis
- K-sparing diuretics reduce both K and H secretion in the collecting tubule
- Avoid if renal failure or on an ACEi
- Good advice to avoid K supplement with the K sparing diuretic
- Hyponatremia
- Diuretics can cause volume depletion leading to enhanced secretion of ADH and to increased water intake
- Almost always due to a thiazide
- Loops destroy the concentrated medullary gradient making ADH less effective
- Hyperdrive is
- Increased urate reabsorption in the proximal tubule
- Process mediated by parallel Na-H and urate OH exchangers see figure 3-13a
- Urate reabsorption varies directly with proximal Na transport and in patients with diuretic-induced volume deficiency both Na and urate excretion are reduced.
- May be related to Ang II
- Do not need to treat the hyperuricemia in asymptomatic patients
- Do not develop urate nephropathy because tubular urateis actually low
- Hypomagnesemia
- Generally mild
- Loop diuretics since most reabsorbed in the loop
- Thiazides don’t affect Mg (why with gitelmans?)
- Hypokalemia may directly inhibit tubular cell mg uptake
- Aldosterone increases Mg excretion, so K sparing diuretics decrease Mg secretion
- Determinants of Diuretic responsiveness
- 2 important determinants of diuretic response
- Site of action
- Presence of counterbalancing antinatriuretic forces
- Ang2
- Aldo
- Low systemic BP
- Adds rate of drug excretion as # 2 and a half
- Almost all diuretics are protein bound
- So not well filtered
- Enter tubule through organic anion and organic cation transporter
- This can limit diuretic effectiveness
- Natriuretic response plateaus at higher rates of diuretic excretion due to complete inhibition of the diuretic target
- This plateau in normal people is 1 mg of bumetanide and 40 mg of furosemide given IV
- Double this for oral furosemide, no adjustment needed for bumetanide
- 15-6
- Refractory edema
- Start with a loop diuretic
- Initial aim is to find the effective single dose
- From the paragraph this is about threshold dosing
- Double ineffective doses until good effect
- Suggests maximum furosemide dose is 200 mg IV and 400 mg oral
- Excess sodium intake
- High sodium diet can work to prevent patients from achieving negative sodium balance.
- Suggests diets after leaving the hospital maybe higher in sodium
- Decreased or delayed intestinal absorption
- Decreased intestinal perfusion, reduced intestinal motility and mucosal edema may contribute.
- But why is this worse with furosemide than with bumetidine or torsemide?
- Decreased drug entry into the tubular lumen
- Thiazides don’t work below a GFR of 20
- CLICK
- Renal failure
- Increased organic anions compete for diuretic secretion
- Bumetidine isn’t as dependent as furosemide on GFR
- Use 1/20th rather than 1/40th the dose
- Maximum of 8 to 10 mg
- Furosemide has ototoxicirty at high doses, he advises against 2400 mg/day
- There is a Na-K-2Cl carrier in the endolymph producing cells
- Ethacrynic acid has the most ototoxicity
- Only loop or thiazide that isn’t a sulfonamide derivative
- Cirrhosis
- Spiro is diuretic of choice
- More effective than loops alone
- Does not induce hypokalemia that can cause hepatic encephalopathy
- Cirrhosis causes marked hyperaldo
- Loop diuretics have to compete with bile salts for secretion in the proximal tubule
- Spiro does not need to be secreted in the proximal tubule
- Recommends to 100 to 40 spiro to furosemide ratio
- And can double this to 200 and 80/day
- and a maximum of of 400/160
- Hypoalbuminemia
- <2 g/dL associated with decreased diuretic entry into the lumen
- Protein binding keeps diuretics in the blood, reduces the volume of distribution
- This maximizes the delivery to the kidney
- In nephrotic syndrome tubular albumin can bind diuretic and prevent its activity
- Co administration of albumin with diuretic has resulted in modest improvements in diuretic effectiveness in various studies
- Intravenous infusion of loop diuretics
- Infusions are greater than bolus
- But if patient is not responding to blouses unlikely to respond to infusions since bolus provides a temporary spike in plasma level
- Increased distal reabsorption
- Increased distal sodium reabsorption decreases the effectiveness of proximal diuretics
- Due to aldo and increased sodium delivery
- Mentions that thiazides have a proximal effect (is that inhibition of carbonic anhydrase?)
- 15-8 is very cool
- Says all thiazides are created equal
- Article from 1972 is why people use metolazone in advanced renal disease
- When doing sequential nephron blocked be careful
- Loss of lots of fluid
- Loss of lots of potassium
- Loss of 5 liters and 200 mEq of K a day is possible with sequential nephron blockade
- Decreased loop sodium delivery
- With heart failure and cirrhosis increased proximal resorption mediated by Ang II markedly reduces delivery of fluid to the diuretic sensitive sites.
- Acetazolamide makes sense here
- Supine or 10 degree head down can increase cardiac output possibly increased venous return
- Can double Na excretion
- Increase CrCl 40%
- CAVH enters the chat!
- Other uses of diuretics
- Met alk, RTA, DI, hyponatremia due to SIADH, hypokalemia
- Diuretics and prostaglandins
- Loops and thiazides increase renal generation of prostaglandins
- Can cause venous dilation may help with acute pulmonary edema
- Can help without increased diuresis
- NSAIDS counter the effect of loop diuretics
- Is this natriuretic effect of PGE? Or due to renal ischemia due to unopposed Ang2 and norepi
- They also raise BP and reduce cardiac output due to increased vascular resistance
- Vasoconstrictor effect of loop diuretics
- One hour after loop diuretics increase vasoconstriction and rise in systemic blood pressure
- Increased Renin and norepinephrine, resolved 4 hours later
- Seen in heart failure and cirrhosis
- In cirrhosis decrease in RPF and GFR of 30-40% with furosemide
Diagnosis and management of Bartter syndrome: executive summary of the consensus and recommendations from the European Rare Kidney Disease Reference Network Working Group for Tubular Disorders https://linkinghub.elsevier.com/retrieve/pii/S0085253820314046
We continued to try to grapple with the work of Jens Titze on sodium which turns many of our assumptions about sodium upside down. His team studied astronauts on a long term high sodium diet and found an unexpected weekly (circaseptan) rhythm seemingly related inversely to aldosterone and directly with cortisol. His work also probes our notion of body sodium content. For a great first hand read, check out Dr TItze’s review in Kidney International 2014 which he aptly dubs, “Spooky Sodium Balence.” https://www.sciencedirect.com/science/article/pii/S0085253815562807
Baroreceptors feature mechanically activated ion channels called PIEZO1 and PIEZO2. Zeng W, Marshall KL, Min S, Daou I, Chapleau MW, Abboud FM. PIEZOs mediate neuronal sensing of blood pressure and the baroreceptor reflex. Science 2018 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5102061/
A series of elegant experiments by Alicia McDonald’s team to characterize pressure natriuresis. In these studies, they induce hypertension by constriction of the superior mesenteric artery, the celiac artery and the infrarenal aorta (essentially increasing afterload without directly altering the blood flow to the kidney). With this maneuver, the blood pressure of the experimental animal rises, urinary sodium excretion increases and then they demonstrate a shift in the Na-H ATPase from the apical membrane to intracellular vesicles in the proximal tubule and a shift in NCC from the luminal membrane to the intracellular vesicles in the distal tubules.
Edelman IS, Leibman J, O’Meara MP and Birkenfeld LW. Interrelations between serum sodium concentration, serum osmolarity and total exchangeable sodium, total exchangeable potassium and total body water. JCI 1958. This classic paper calculates the total body exchangeable sodium and potassium and establishes the relationship between these. Understanding this painstacking work helps understand the effect of supplementing potassium in the setting of hyponatremia.
in this exciting exploration of the basic assumptions that we hold true regarding salt and water (and staring Russian cosmonauts and an incredible controlled simulation of salt and water intake), Titze shows that high sodium intake does not simply drive water consumption (as we usually teach) but instead leads to a complex hormonal and metabolic response (even with diurnal variation!) and results in body water conservation and decreased water consumption.
In addition, Titze and others have done interesting work on sodium deposition in tissues where it may also be a source for systemic inflammation.https://pubmed.ncbi.nlm.nih.gov/28154199/
A discussion/debate of the overfill vs. underfill theory of edema in the nephrotic syndrome (hint- overfill theory triumphs) would be incomplete without a reference to congenital analbuminemia. This reference from Frontiers in Genetics explores the diagnosis, phenotype and molecular genetics and reveal that patients tend to have only mild edema but severe hyperlipidemia. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6478806/
The finding that proteinuria can directly lead to sodium retention based on a study when puromycin aminoglycoside induced proteinuria of one kidney lead to sodium retention by that kidney which was localized to the distal nephron. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC436841/?page=9
Under protest, we hobbled through a discussion of the Gibbs Donnan affect even encouraged by one of Amy’s fellows based on this article from QJM: https://academic.oup.com/qjmed/article/101/10/827/1520972 suggesting that our understanding of the role of hyponatremia in fractures might be all wrong- it could be related to hypoalbuminemia.
We wondered/debated on our observation that hyponatremia is not reliably seen in patients receiving vasopressin in the ICU. In the VASST trial, Vasopressin versus Norepinephrine Infusion in Patients with Septic Shock, 1 patient in each study arm of nearly 400 patients developed hyponatremia. Note that patients with hyponatremia (<130 mEq/L) were excluded from the study.
Here’s a little discussion of Dr. Grant Liddle. In addition to his eponymous syndrome, he coined the term “ectopic” and developed the dexamethasone suppression test.Grant Liddle (1921–1989) : The Endocrinologist
We wondered/debated on our observation that hyponatremia is not reliably seen in patients receiving vasopressin in the ICU. In the VASST trial, Vasopressin versus Norepinephrine Infusion in Patients with Septic Shock, 1 patient in each study arm of nearly 400 patients developed hyponatremia. Note that patients with hyponatremia (<130 mEq/L) were excluded from the study.
Here’s a little discussion of Dr. Grant Liddle. In addition to his eponymous syndrome, he coined the term “ectopic” and developed the dexamethasone suppression test.Grant Liddle (1921–1989) : The Endocrinologist
If you love diuretics, you will love this classic paper from Craig Brater on diuretics Diuretic Therapy | NEJM which also includes the t1/2 of various diuretics and points out that chlorthalidone’s half life is 24-55 hours so eliminated after 4-10 days.
We ended on a high note when we considered the urothelium of the American black bear. These magnificent creatures have aquaporins 1 &3 that allow them to reabsorb their own urine during hibernation. The urothelium of a hibernator: the American black bear
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