Kidney Capacity and Function

anonymous@undisclosed.example.com (Anonymous) — Wed, 14 Sep 2022 06:37:14 +0000

10.12.2018		current
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	===== Further reading =====		===== Further reading =====

-	Elevations in serum creatinine with RAAS blockade: why isn't it a sign of kidney injury? (({{pubmed>long:18695383}}))	+	Elevations in serum creatinine with RAAS blockade: why isn't it a sign of kidney injury? (({{pmid>long:18695383}}))

-	Long-term effects of olmesartan, an Ang II receptor antagonist, on blood pressure and the renin-angiotensin-aldosterone system in hypertensive patients. (({{pubmed>long:11768722}}))	+	Long-term effects of olmesartan, an Ang II receptor antagonist, on blood pressure and the renin-angiotensin-aldosterone system in hypertensive patients. (({{pmid>long:11768722}}))

-	Role of renin-angiotensin system in inflammation, immunity and aging. (({{pubmed>long:22283774}}))	+	Role of renin-angiotensin system in inflammation, immunity and aging. (({{pmid>long:22283774}}))

-	Changeover Trial of Azilsartan and Olmesartan Comparing Effects on the Renin-Angiotensin-Aldosterone System in Patients with Essential Hypertension after Cardiac Surgery (CHAOS Study). (({{pubmed>long:27086671}}))	+	Changeover Trial of Azilsartan and Olmesartan Comparing Effects on the Renin-Angiotensin-Aldosterone System in Patients with Essential Hypertension after Cardiac Surgery (CHAOS Study). (({{pmid>long:27086671}}))
	===== Giving the kidneys chance to recover =====		===== Giving the kidneys chance to recover =====

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	==== Activation of RAS ====		==== Activation of RAS ====

-	from Nangaku M et al. J Am Soc Nephrol. (2006) (({{pubmed>long:16291837}}))	+	from Nangaku M et al. J Am Soc Nephrol. (2006) (({{pmid>long:16291837}}))

	<blockquote>Among various vasoactive substances, local activation of RAS is especially important because it can lead to constriction of efferent arterioles, hypoperfusion of postglomerular peritubular capillaries, and subsequent hypoxia of the tubulointerstitium in the downstream compartment. To clarify the mechanism of these effects, we used a remnant kidney model in rats induced by ligation of renal artery branches, in which RAS is markedly activated. Our computer-assisted morphologic analysis demonstrated narrowing and distortion of peritubular capillaries with decreased blood flow and hypoxia in a very early phase in this model, before the development of structural kidney damage (37). In addition, angiotensin II damages endothelial cells directly: Administration of angiotensin II to rats causes the loss of peritubular capillaries, an effect that is ameliorated by receptor blockade (38,39). A second important mechanism of angiotensin II–induced ischemia is inefficient cellular respiration and hypoxia via oxidative stress, which is detailed below. Thus, angiotensin II induces tubulointerstitial hypoxia via both hemodynamic and nonhemodynamic mechanisms. Intrarenal vasoconstriction may also occur secondary to increased local endothelin or a local loss of vasodilating nitric oxide (NO).</blockquote>		<blockquote>Among various vasoactive substances, local activation of RAS is especially important because it can lead to constriction of efferent arterioles, hypoperfusion of postglomerular peritubular capillaries, and subsequent hypoxia of the tubulointerstitium in the downstream compartment. To clarify the mechanism of these effects, we used a remnant kidney model in rats induced by ligation of renal artery branches, in which RAS is markedly activated. Our computer-assisted morphologic analysis demonstrated narrowing and distortion of peritubular capillaries with decreased blood flow and hypoxia in a very early phase in this model, before the development of structural kidney damage (37). In addition, angiotensin II damages endothelial cells directly: Administration of angiotensin II to rats causes the loss of peritubular capillaries, an effect that is ameliorated by receptor blockade (38,39). A second important mechanism of angiotensin II–induced ischemia is inefficient cellular respiration and hypoxia via oxidative stress, which is detailed below. Thus, angiotensin II induces tubulointerstitial hypoxia via both hemodynamic and nonhemodynamic mechanisms. Intrarenal vasoconstriction may also occur secondary to increased local endothelin or a local loss of vasodilating nitric oxide (NO).</blockquote>
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	Another citation reports inhibition of STAT1 by binding with unliganded VDR.		Another citation reports inhibition of STAT1 by binding with unliganded VDR.

-	[[http://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0078695&type=printable\|NF-kB and CREB Are Required for Angiotensin II Type 1 Receptor Upregulation in Neurons]]	+	[[https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0078695&type=printable\|NF-kB and CREB Are Required for Angiotensin II Type 1 Receptor Upregulation in Neurons]]

-	[[http://www.jimmunol.org/content/early/2014/05/10/jimmunol.1302296\|Vitamin D Receptor and Jak–STAT Signaling Crosstalk Results in Calcitriol-Mediated Increase of Hepatocellular Response to IFN-α]]	+	[[https://www.jimmunol.org/content/early/2014/05/10/jimmunol.1302296\|Vitamin D Receptor and Jak–STAT Signaling Crosstalk Results in Calcitriol-Mediated Increase of Hepatocellular Response to IFN-α]]


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	https://www.youtube.com/watch?v=BVUeCLt68Ik Khan academy (14 min.)		https://www.youtube.com/watch?v=BVUeCLt68Ik Khan academy (14 min.)

-	--- //Sallie Q 02.17.2017// created page arranging material posted by Jigsaw and approved by him	+

	RAS refs		RAS refs
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	other refs went to, one went nowhere		other refs went to, one went nowhere
-	http://www.kidney-international.org/	+	https://www.kidney-international.org/
-	also CO2 blood test http://www.kidney-international.org/ for elsewhere if not there	+	also CO2 blood test https://www.kidney-international.org/ for elsewhere if not there
-	& Hyperkalemia http://www.medicinenet.com/hyperkalemia/page4.htm	+	& Hyperkalemia https://www.medicinenet.com/hyperkalemia/page4.htm

-	hyper K management http://www.fpnotebook.com/renal/potassium/hyprklmmngmnt.htm	+	hyper K management https://www.fpnotebook.com/renal/potassium/hyprklmmngmnt.htm
	Bicarbonate supplementation slows progression of CKD and improves nutritional status.		Bicarbonate supplementation slows progression of CKD and improves nutritional status.
	https://www.ncbi.nlm.nih.gov/pubmed/19608703		https://www.ncbi.nlm.nih.gov/pubmed/19608703
	Metabolic Acidosis		Metabolic Acidosis
-	http://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/acid-base-regulation-and-disorders/metabolic-acidosis	+	https://www.merckmanuals.com/professional/endocrine-and-metabolic-disorders/acid-base-regulation-and-disorders/metabolic-acidosis
	** Mechanism of acid-induced bone resorption. 15199293 15199293		** Mechanism of acid-induced bone resorption. 15199293 15199293
	Metabolic, but not respiratory, acidosis increases bone PGE2 levels and calcium release 11704556		Metabolic, but not respiratory, acidosis increases bone PGE2 levels and calcium release 11704556

-	hyper K http://emedicine.medscape.com/article/241185-overview#a0104	+	hyper K https://emedicine.medscape.com/article/241185-overview#a0104
-	hyper K http://www.unitedhealthdirectory.com/diseases-and-conditions/hyperphosphatemia/	+	hyper K https://www.unitedhealthdirectory.com/diseases-and-conditions/hyperphosphatemia/


-	tetany [defn] http://www.medicinenet.com/script/main/art.asp?articlekey=13312	+	tetany [defn] https://www.medicinenet.com/script/main/art.asp?articlekey=13312
	https://en.wikipedia.org/wiki/Tumor_lysis_syndrome		https://en.wikipedia.org/wiki/Tumor_lysis_syndrome


		+	===== References =====

Marshall Protocol Knowledge Base - home:special:kidneys_at_work

Kidney Capacity and Function