Water
How much water?
Drinking a lot of water (3-4 Liters) throughout the day reduces vasopressin levels. Drinking before each laboratory test may have a similar effect as tolvaptan, the new drug approved for PKD. PKD medical research points to the possibility that by increasing water intake, we can slow down kidney decline and cyst growth. Some have tried increasing water intake to 3 - 4 liters/day. This shuts down vasopressin decreasing kidney cyst growth. If your doctor has restricted water intake for any reason, continue to follow your doctor's advice.Low Osmolar Diet and Adjusted Water Intake for Vasopressin Suppression in ADPKD
This is a clinical water trial at Tufts University with Dr. Perrone. Its title is Diet as a Potential Treatment for Autosomal Dominant Polycystic Kidney Disease.Water a possible treatment for PKD?
PKD Clinical trials for increasing daily drinking of water have begun. The results of the PKD water clinical trial are here Other doctors in Japan are also looking at water as a treatment for PKD. There completed water trial in Kansas City, USA.In the PKD model, drinking enough water to shut down vasopressin has resulted in a reduction in plasma vasopressin levels; renal cyst cell proliferation decreased; and in the rats who increased their water intake, their progression of PKD diminished. Cyst growth diminished. These PKD models developed smaller cystic kidneys with a lower number of kidney cysts.
Sustained hydration might be beneficial to PKD’rs especially early in the disease by shutting down the detrimental effects of vasopressin (similar to taking tolvaptan).
The rats drank the equivalent of 20 liters of water per day. Large human clinical trials are certainly warranted. This works in both ADPKD and ARPKD. No one can give an answer as to how much water should PKD’rs drink, but common sense says sufficient water intake would be to keep plasma vasopressin levels near a point that renders urine osmolality equal to or modestly lower than that of plasma. To know for certain how much of the water cure is prudent therapy, a carefully controlled clinical trial seems justified. Many of us have tried drinking 3 liters/ day. Others have tried increasing their intake to 8 liters/day. We have yet to see if this makes a difference.
Increased Water Intake Decreases Progression Polycystic Kidney Disease PCK Rat
Wallace D 2006 J Am Soc Nephrol 17: 2220–2227, 2006. doi: 10.1681/ASN.2006030251
Arginine vasopressin (AVP) is an important antidiuretic hormone that mediates its effect through the activation of vasopressin V2 receptors (AVPV2R) and the subsequent stimulation of adenylyl cyclase and synthesis of cAMP (10). . .Normally, urine is concentrated to an osmolality that is greater than plasma. Day-to-day maintenance of urine output depends on appropriate plasma AVP levels to regulate osmotic water reabsorption by distal tubules and collecting ducts. Relatively normal plasma levels of AVP may be sufficient to stimulate cyst epithelial cell growth and renal enlargement in patients with PKD. Some patients have an intrinsic defect in the capacity to concentrate urine maximally, potentially leading to even greater levels of plasma AVP than normal (11–13). .Increased water intake sufficient to cause a reduction in plasma (arginine vasopressin) AVP levels decreased renal cell proliferation, and slowed PKD progression in PCK rats. We propose that sustained hydration by increased water intake may be beneficial to some patients with PKD by limiting the detrimental effects of (arginine vasopressin) AVP on renal cyst growth.
Water for ADPKD? Probably, Yes
Torres V E 2006 Am Soc Nephrol 17: 2089–2091,
2006. doi: 10.168 1/ASN 2006060 60 3
Increased fluid intake may be beneficial to some patients with ADPKD, at least in early stages of the disease. . If increased fluid intake, either by itself or together with the administration of V2 receptor antagonists, is proved to slow the rate of growth of polycystic kidneys, then its long-term safety will need to be considered. . . .A number of studies of other possible treatments for PKD have been published during 2005 to 2006. Long-acting octreotide may inhibit cAMP production. . .Rapamycin, an inhibitor of mammalian target of rapamycin (32–34), have been effective in animal models of cystic disease. The pace of development of new potential therapies for ADPKD raises the hope that its inexorable clinical course soon may be modified. .Caffeinated beverages should be discouraged because caffeine inhibits phosphodiesterase; enhances cAMP accumulation; and potentates the effects of vasopressin on chloride secretion, cell proliferation, and cyst growth, at least in vitro . . Calorically sweetened beverages and fruit drinks are major contributors to the epidemic of obesity in the United States and should be avoided. Because drinking tap water has been associated in some studies with a slightly increased risk for bladder cancer in men, whereas non-tap water has not, high-quality or bottled water may be preferable . . .A retrospective analysis of the MDRD study (139 participants with and 442 without ADPKD; GFR at entry 25 to 55 ml/min per 1.73 m2) was performed to examine the relationship between fluid intake (reflected by 24-h urine volume and urine osmolality) and renal disease progression. Higher urine volumes and lower urine osmolality is associated with faster GFR decline regardless if the patient had ADPKD. The authors considered two possible explanations. The first was that excessive fluid intake and high urine volume cause faster renal disease progression and possibly cyst growth in ADPKD. The second was that high urine volume with low urine osmolality is the result and not the cause of faster renal disease progression. The results by Nagao et al. do not support the first explanation; on the contrary, they suggest that increased fluid intake may be beneficial to some patients with ADPKD, at least in early stages of the disease. . .Long-acting octreotide may inhibit cAMP production, and a pilot study of patients with ADPKD has shown promising results. PD184352, an inhibitor of mitogen-activated protein kinase/ extracellular signal–regulated kinase, and rapamycin, an inhibitor of mammalian target of rapamycin, have been effective in animal models of cystic disease. The pace of development of new potential therapies for ADPKD raises the hope that its inexorable clinical course soon may be modified.
Vasopressin Directly Regulates Cyst Growth in Polycystic Kidney
Torres V E 2008 Am Soc Nephrol. 2008 Jan;19(1):102-8. Epub 2007 Nov 21.
These observations indicate that AVP is a powerful modulator of cystogenesis and provide further support for clinical trials of V2 receptor antagonists in PKD.
Therapy for Polycystic Kidney Disease? It’s Water
Grantham JJ 2008 J Am Soc Nephrol 19: 1–2, 2008. doi: 10.1681/ASN.2007101100
Now we are confronted by the bizarre prospect that water is the“cure” for hereditary diseases that grotesquely bloat the kidneys with . . . water. . .Cysts arise in renal tubules when epithelial cells focally proliferate, leading to tiny outpouchings, that progressively expand, upstream fluid from glomerular filtrate fills the budding cyst cavity. Later, after they separate from the parent tubules. Two ordinarily quiescent renal processes, epithelial cell proliferation and solute-driven fluid secretion, come storming out of hiding and push a relatively small number of cystic segments to take over eventually the parenchymal landscape, driving functional glomeruli and tubules into oblivion. .We knew this much about PKD for more than a decade. . .Although studies clearly implicate a central role for vasopressin and cAMP in promoting kidney enlargement and reducing renal function in PKD, a study from the Mayo laboratory in this issue of the JASN9 provides definitive proof. The dramatic results in this report are consonant with the view that epithelial cell growth is of paramount importance to the formation of the cyst as well to the overall increase of renal size in ARPKD. . .Of the hormones capable of increasing cAMP production in collecting ducts, only AVP (arginine vasopressin) is persistently elevated in the plasma of humans. Where do the cysts form in ARPKD? In collecting ducts. Land based animals are normally antidiuretic for most hours of the day and night, except for short periods when relatively large volumes of water are imbibed. Therefore, plasma AVP levels are usually high enough to activate adenylyl cyclase, generate cAMP, activate aquaporin-2, increase collecting duct permeability to water, and concentrate urinary osmolality above that of plasma. Thus, cyst growth is “clamped” by vasopressin. . .How much water should I drink now? Patients have already figured out that if extra water decreases vasopressin and cAMP levels, then why isn’t plain old water a useful therapy? No one can give an informed, definitive answer to that question, but common sense leads me to think that sufficient water should be drunk to keep plasma vasopressin levels near a point that renders urine osmolality equal to or modestly lower than that of plasma. To know for certain how much of the “water cure” is prudent therapy, a carefully controlled clinical trial seems justified.
Water Prescription for PKD
Clin J Am Soc Nephrol. 2011 Jan;6(1):192-7. Epub 2010 Sep 28.
Design, setting, participants, & measurements In eight ADPKD patients eating typical diets, osmolality and volume were measured in 24-hour urine collections. The amount of additional ingested water required daily to achieve a mean urine osmolality of 285 ± 45 mosm/kg was determined. Participants were instructed to distribute the prescribed water over waking hours for each of 5 days. Blood chemistries, 24-hour urine collections, BP, and weight were measured before and after the period of supplemental water intake. Results Five patients achieved the 285 mosm/kg urine target without difficulty. Mean urine osmolality decreased and mean urine volume increased; serum sodium, weight, and BP were unchanged. Daily osmolar excretion remained constant, indicating a stable ad lib dietary intake of solutes and protein over the 2-week study period. Conclusions The amount of additional water needed to achieve a urine osmolality target can be approximated from the urine osmolar excretion in ADPKD patients eating typical diets, providing a quantitative method to prescribe supplemental water for such individuals.
Effects of lovastatin rat model PKD
Klawitter et al. BMC Nephrology 2013, 14:165 http://www.biomedcentral.com/1471-2369/14/165
Lovastatin was able to decrease kidney weight and cyst volume density in Cy/+ rats. The decrease in cyst volume was accompanied by a reduction in arachidonic acid-mediated inflammation markers, the normalization of metabolism of NO precursors and the improvement of kidney energy cell metabolism.
Limited water trial Japan
Does increased water intake prevent disease progression in autosomal dominant polycystic kidney disease?
Eiji Higashihara, MD
Professor Department of Urology
Kyorin University School of Medicine
"The urine volume was greater in those drinking 2.5-3 L daily than those allowed free to access water intake. Data including total kidney volume and kidney function were not significantly different between the two groups."
According to the article:
There was no difference in kidney functioning between the two groups.
What was the amount of water drunk by the free water drinking group?
In those who had an increase in kidney volume, did anyone have less than 5% per year change in kidney volume?
This finding would be significant. Was the water drunk tap water? Did the tap water contain dichloroacetate, a contaminant from water chlorination.
Once ADPKD kidneys begin to decline, the expected rate of decline is 5% per year. With declining PKD kidneys, urine volume will temporarily increase for a short time (kidneys fail to concentrate urine); then urine volume will diminish sometimes to seemingly no urine output at all.
How many from each group experienced diminished kidney functioning at a rate of less than 5% per year?
An estimated eGFR kidney functioning was done when a creatinine clearance or a standard GFR would have been preferable.
Were the two groups matched by age, sex and kidney functioning? This trial leaves one with more questions than answers.
By the two groups not being matched, the Kidney function and Total Kidney Volumes worsening is not understandable.
If one group had a greater age or slightly lower kidney functioning, then this finding could then be
comprehended. Not enough parameters were looked at; not enough information is given. This article discusses
the importance of matching participants
in a PKD trial
Eliminating Fluoride in city water
First find out if your water is fluoridated by contacting your local water department. Or if you live in the U.S., try fluoride alert. From the pulldown menu on the fluoride alert website, select your state to see answers regarding your state.Water filters that remove fluoride
reverse osmosis
deionizer (which use ion-exchange resins)
activated alumina (avoid)
Each of these filters can remove about 90% of existing fluoride.
By contrast, activated carbon
filters (e.g., Brita & Pur) do not remove fluoride.
Anyone tried OKO or a Clear2Go water bottle filter?
For home use reverse osmosis seems the best option for fluoride free drinking water.
This tiny star is a droplet of water that formed after
it was exposed to the word Truth.
The droplet was then frozen and later photographed.
Water Filters
Carbon filters will help eliminate lead and reverse osmosis filters will help decrease dioxin levels in water. Dioxin is a known carcinogen.City Water
2013 Oklahoma wins the best tasting tap water. The second best tasting city water is in Minnesota. EWG rates water for some USA cities.Dichloroacetate DCA in tap water
Dichloroacetate is a common contaminant in the drinking water supply which has been chlorine in city water. One can leave tap water out for 24 hours to dissipate the chlorine. Others have tried the use of a water filter that eliminates chlorine.When skin cells are warmed and dilated like when in a hot shower, there is increased chlorine absorption as well as the contaminant dichloroacetate. Some have used shower filters to deter this mechanism from happening.
Scientists have discovered that dichloroacetate can increase cyst development. Dichloroacetate was detected in some tap waters. The contaminant from chlorination, dichloroacetate, could possibly account for the differing results from drinking water studies in ADPKD.
2014
The advantages of drinking water early in the treatment of ADPKD is explained in an article by Dr. Grantham.↑ water intake PKD
From the above article:
"Although evidence is lacking to support increased water intake in the general population, available evidence
indicates that individuals who are at risk for nephrolithiasis as well as those with CKD and PKD may benefit
from 3-4 Liters of urine output each day, a level of excretion that is likely to be safe."
Keep Your Kidneys Healthy
Diet
PKD Treatments
PKD Research
Monitor alkalinity
Monitor protein
Monitor Blood Pressure
Monitor Water Intake
Increasing water intake for some can improve PKD kidney health
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