Below you will find pages that utilize the taxonomy term “physiology”
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Curvilicious
In this post… The Brenner hypothesis Tubuloglomerular feedback & glomerulotubular balance How SGLT2i affect glomerular haemodynamics How loop diretics effect glomerular haemodynamics The importance of intraglomerular pressure At the cornerstone of contemporary treatments to delay CKD progression are agents (RAS inhibitors and SGLT2i) that reduce intraglomerular pressure. Whether or not this effect is the most important mechanism of nephroprotection is open to debate - particularly for SGLT2i. However, it is at the very least likely to be a central mechanism.
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Bicarbonaturia
In this post… The renal regulation of bicarbonate excretion
The pathogenesis of proximal RTA
The pathophysiology of vomiting How is renal bicarbonate excretion regulated? With respect to bicarbonate reabsorption, there are two key parameters to consider: the Tm = maximal rate of tubular HCO3 reabsoption and the renal bicarbonate threshold = the serum [HCO3] at which the filtered load exceeds Tm, and bicarbonate begins to appear in the urine.
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A tonic for hyponatraemia
In this post… The etymology of “tonic”.
Is urea an effective osmole?
The anatomy of the EFWC equation.
How do NaCl supplements help in hyponatraemia? tonic, adj. and n. Medicine, etc. Having the property of increasing or restoring the tone or healthy condition and activity of the system or organs; strengthening, invigorating, bracing. (Of remedies or remedial treatment, and hence of air, climate, etc.) Etymology: Greek of or for stretching
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Dietary salt: clinical pearls
In this post… A summary of our recent salt perspectives paper A few “clinical pearls” relating to salt Introduction We (with Matt Bailey and Bean Dhaun) recently wrote a perspectives article on salt and disease. This was an entertaining and educational process. Here I reflect on what I learned while writing the review, expanding a little on some potentially useful “clinical pearls”.
(As the following is discussed in detail and fully referenced in our paper, I have not inserted many references below.
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The E=mc2 of nephrology
In this post… Why drinking seawater causes dehydration
Why giving 0.9% NaCl can exacerbate hyponatraemia in some circumstances
How much water do you have to drink to cause hyponatraemia
Why most patients on furosemide should also have restricted water intake
Why a “tea and toast” diet causes hyponatraemia
Why limiting dietary solute intake can help in nephrogenic diabetes insipidus Physicists may still be searching for the grand unified theory of everything, but nephrologists have come pretty close to a unified theory of urine.
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When is a diuretic not a diuretic?
In this post… The paradoxical anti-diuretic effects of diuretics
A general approach to nephrogenic diabetes insipidus When is a tractor not a tractor?
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When it turns into a field
Nephrogenic diabetes insipidus Nephrologists are often asked for advice on how to manage patients with nephrogenic diabetes insipidus (NDI). Almost always, this has been caused by current or historic lithium exposure.
This is one of those referrals that invariably sends me scuttling back to review original literature, because I can never quite remember how on earth diuretics are supposed to magically transform into anti-diuretics in this context, nor the relative merits of thiazides / amiloride / acetazolamide.
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Oh Mg (part 2)
In this post… Why does low Mg cause low K?
Distal Na and K transport and the transepithelial voltage Hypomagnesaemia: easy to find if you go looking for it; usually left well alone. (And often caused by a drug.)
But sometimes hypomagnesaemia is worth paying attention to if it is contributing to another electrolyte disorder such as hypocalcaemia or hypokalaemia. Any medical student can tell you that Mg deficiency can cause refractory hypokalaemia.
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Should I stop the furosemide?
In this post… What effect do loop diuretics have on renal free water clearance?
Should we stop furosemide in hyponatraemia?
Why do we need to restrict water intake when giving furosemide in hyponatraemia? We are mostly water and rapidly run into trouble when we become under- or over-hydrated. We could argue, therefore, that one of the kidney’s most important jobs is that of maintaining water homeostasis. It is surprising that we are able to mess around quite profoundly with this process without running into trouble more frequently than we do.
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Terlipressin and hyponatraemia
In this post… The evolution of the vasopressin system
How can one hormone regulate two physiological parameters (tonicity and blood pressure)?
Why does terlipressin not always cause profound hyponatraemia? “Thousands have lived without love, not one without water.”
— WH Auden
Does terlipressin cause hyponatraemia? We had a patient with hepatorenal syndrome on the unit recently. Her sodium was 125 mM and I found myself wondering - as I always do in such a patient - whether terlipressin could be contributing.
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Sugar and spice and all things nice
In this post… Electrolyte-free water clearance can help assess disorders of sodium homeostasis
Potassium supplementation can help in cases of hyponatraemia What are we made of? What are little girls made of?
What are little girls made of?
Sugar and spice
And all things nice
That’s what little girls are made of
— Nursery Rhyme
Well we are not made of sugar and spice - but what are we made of?
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Filtration-reabsorption: the central renal paradox
In this post… How the kidney evolved to filter first and reabsorb later
How we came to know how the kidney works in this way It is so obvious! ‘One never notices what has been done; one can only see what remains to be done.’
— Marie Curie
As facts become established dogma, it becomes almost impossible to conceive of a time when they were not known. How could we have not known about natural selection before Darwin?