Urinary Concentration and Dilution in the Aging Kidney

During normal aging, there is a decrease in maximal urine concentrating ability [1-3]. This physiological change was clearly demonstrated by the Baltimore Longitudinal Study of Aging [1]. Rowe and colleagues measured maximal urine concentrating ability in healthy individuals in three age groups: 20−39, 40−59, and 60−79. Individuals aged 60−79 had approximately a 20% reduction in maximum urine osmolality, a 50% decrease in the ability to conserve solute, and a 100% increase in minimal urine flow rate, when compared to the two younger age groups [1]. The change in urine concentrating ability could not be explained by a decrease in glomerular filtration rate [1]. Aged individuals do have a diminished thirst response, but the relationship between vasopressin (also named antidiuretic hormone) secretion and plasma osmolality is preserved and may even be enhanced [3]. Thus, neither a reduction in renal function, as measured by glomerular filtration rate, nor an abnormality in vasopressin secretion, appears to be the mechanism that explains the decrease in urine concentrating ability during aging [1;3;4]. The cloning (reviewed in [5-7]) of many of the key renal medullary water (aquaporins) and solute (sodium and urea) transport proteins that are involved in the urine concentrating mechanism, and the type 2 vasopressin receptor, have resulted in studies into the molecular mechanisms underlying the reduction in urine concentrating ability that occurs during aging.


Urine Concentrating Mechanism
The region of the kidney that is responsible for the generation of concentrated or dilute urine is the medulla (figure 1). To produce a concentrated urine, the collecting duct must be permeable to water and a hypertonic medullary interstitium must be generated by the nephron segments located in the loops of Henle (reviewed in [8;9]). To generate a hypertonic medullary interstitium, a small osmotic gradient is generated at each level of the medulla and then magnified down its length by countercurrent multiplication. In the thick ascending limb of the loop of Henle (in the outer medulla): the NKCC2/BSC1 cotransporter actively reabsorbs Na+, K+, and Cl− across the apical membrane; the K+ that is reabsorbed is secreted back into the lumen via the K+ secretory channel ROMK; resulting in net NaCl reabsorption.

Transport proteins involved in the urinary concentrating mechanism. In the outer medulla, active NaCl reabsorption via NKCC2/BSC1 in the thick ascending limb of the loop of Henle generates a hypertonic medullary interstitium. This concentrates NaCl in ...
In contrast to the outer medulla, NaCl is passively reabsorbed in the inner medulla across the thin ascending limb of the loop of Henle (reviewed in [8;9]). The thin ascending limb luminal fluid has a higher concentration of NaCl and a lower concentration of urea than inner medullary interstitial fluid, thereby establishing chemical gradients that favor NaCl reabsorption and urea secretion, provided that the interstitial urea concentration is sufficiently high. NaCl reabsorption exceeds urea secretion in the thin ascending limb, as it has a higher permeability to NaCl than urea, thereby resulting in dilution of the thin ascending limb luminal fluid as it ascends towards the outer medulla.

NaCl reabsorption in both ascending limb portions of the loop of Henle results in both: a hypertonic medullary interstitium; and delivery of a dilute fluid (relative to plasma) to the distal tubule since both ascending limb segments are water impermeable. The collecting duct is impermeable to water in the absence of vasopressin, resulting in excretion of this dilute fluid as dilute urine. However, the collecting duct becomes highly permeable to water in the presence of vasopressin, and if a hypertonic medulla is present, water is reabsorbed resulting in excretion of a concentrated urine (reviewed in [8;9]).

Vasopressin Receptors
There are two types of vasopressin receptors: type 1 and type 2 (reviewed in [10]). The V2-receptor is involved in urinary concentration. It is expressed in the collecting duct, is a G-protein coupled 7 transmembrane spanning receptor, and its activation results in the generation of the second messenger cyclic AMP. The V1-receptor is involved in increasing systemic blood pressure and has two subtypes: V1a and V1b (also called V3). It is expressed in vasculature, liver, and brain, and its activation results in the generation of the second messenger intracellular calcium.

Water reabsorption along the entire collecting duct is regulated by vasopressin binding to the V2-receptor and stimulating cAMP production (reviewed in [5;9;11]). When blood plasma osmolality becomes elevated by water deprivation (or other causes), hypothalamic osmoreceptors, which can sense an increase of as little as 2 mOsm/kg H2O, stimulate vasopressin secretion from the posterior hypothalamus. Vasopressin binds to V2-receptors in the basolateral plasma membrane of collecting duct principal cells and IMCD cells, which stimulates adenylyl cyclase to produce cAMP and in turn activates protein kinase A.

One potential mechanism for the aging-related decrease in urine concentrating ability would be a reduction in V2-receptors in the aged kidney. In rat, a decrease in V2-receptor mRNA abundance has been detected in one study [12] but no effect on V2-receptor mRNA abundance or vasopressin-stimulated cAMP production was detected in other studies [13-15]. Thus, there is conflicting data on the effect of aging on V2-receptor mRNA abundance (and no data on V2-receptor protein abundance).

Aquaporins
At present, there are 13 cloned water channels or aquaporins (AQPs), 6 of which are expressed in the kidney (reviewed in [5;9]). AQP1 is expressed in the proximal tubule and descending limb of the loop of Henle; AQP7 is also expressed in the proximal tubule. AQP2 is expressed in the apical plasma membrane and sub-apical vesicles of the collecting duct and is the “vasopressin-regulated” water channel. AQP3 and APQ4 are expressed in the basolateral plasma membrane of the collecting duct. AQP6 is expressed in intracellular vesicles in the collecting duct in association with H+-ATPase.

The primary mechanism by which vasopressin rapidly regulates water reabsorption in the collecting duct is by regulating the accumulation of AQP2 in the apical plasma membrane (reviewed in [5;9]). Vasopressin regulation involves both AQP2 phosphorylation at serines 256, 261, 264, and 269 [16-19], and regulated trafficking of AQP2 between sub-apical vesicles and the apical plasma membrane (reviewed in [5]). Wade and colleagues [20] originally proposed the “membrane shuttle hypothesis” in 1979, at a time when water channels had not been cloned or identified. They proposed that the (putative) water channels were stored in vesicles and inserted exocytically into the apical plasma membrane in response to vasopressin. After AQP2 was cloned, the “membrane shuttle hypothesis” was confirmed experimentally by Knepper and colleagues in rat inner medullary collecting ducts (reviewed in [5]). The water that is reabsorbed through AQP2 exits the collecting duct principal cells through AQP3 and AQP4. Water reabsorption is stopped when vasopressin-stimulation ends by endocytosing AQP2 back into the cell, where it is recycled into endosomes until the next stimulation by vasopressin (reviewed in [5;9]).

Several studies show that the protein abundance of some AQPs is reduced in the aged rat kidney [13;21], which could contribute to the reduction in concentrating ability during aging. These studies show that AQP2 protein abundance is reduced in 24−30 month-old rats (which are very old rats), when compared to 10 month-old rats, in both the outer and inner medulla [12;13;21]. The abundance of AQP2 that is phosphorylated at serine 256 is also markedly reduced in the older rats [21]; phosphorylation of serines 261, 264, and 269 has not been studied to date. AQP3 protein abundance is also reduced in the inner medulla of 30 month-old rats, compared to 10 month-old rats, but not in the outer medulla [13;21]. Transepithelial water reabsorption across the collecting duct of aged rats is likely to be reduced by the reductions in AQP2 and AQP3 protein abundances. These changes appear to be specific for AQP2 and AQP3 since neither AQP4 nor AQP1 protein abundances differ between 30 and 10 month-old rats [13;21;22].

The preceding studies pertain to the basal state, ie. rats receiving food and water ad libitum. An important clinical issue is the response of aged people to dehydration, as elderly individuals are more susceptible to dehydration than younger individuals. To model this situation in rats, we compared the ability of 30 month-old rats to respond to 3 days of water restriction, as compared to the response of 4 month-old rats [23]; 4 month-old rats are young adult animals (figure 2). Both the 30 and 4 month-old rats lost 8% of their body weight and had similar increases in hematocrit, but only the older rats became hypernatremic [23]. AQP2 protein abundance and urine osmolality increased significantly in the 4 month-old rats but not in the 30 month-old rats [12;23;24]. Somewhat surprisingly, AQP2 protein abundance did not increase in dehydrated 15 month-old rats, similar to the response in the 30 month-old rats [24]. AQP2 mRNA abundance also increased in dehydrated 2 month-old rats but not in dehydrated 7 month-old rats [14]. Thus, the age at which concentrating ability is lost in rats may be significantly younger than 24−30 months.

Water restriction does not increase AQP2 protein abundance in 30 or 15 month-old rats. Panel A: densitometic summary. There was no significant difference between hydrated (Hyd.) vs. dehydrated (Dehyd) in the 30 or 15 month-old rats. Asterisk indicates ...
The preceding studies suggest that an important mechanism that contributes to the reduction in urine concentrating ability in aging is a failure to increase AQP2 protein abundance in the collecting duct in response to vasopressin. To determine whether this defect could be corrected pharmacologically, supra-physiologic concentrations of dDAVP (Desmopressin), a selective V2-receptor agonist that does not increase blood pressure, were administered to 30 and 10 month-old rats [25]. dDAVP administration caused similar increases in urine osmolality and decreases in urine flow rate in 30 and 10 month-old rats, although the maximum urine osmolality in the older rats was lower than in the younger rats [25]. dDAVP administration also increased the protein abundances of both AQP2 and AQP3 [25], suggesting that the reduced maximal urine osmolality in the aged rats is related, at least in part, to the reduced level of these AQP proteins.


Sodium Transporters
NaCl reabsorption through the Na+-K+-2Cl− cotransporter NKCC2/BSC1 is critical for the establishment of the hypertonic medullary interstitium that is needed to concentrate urine (reviewed in [8;9]). NKCC2/BSC1 protein abundance is reduced in older rats in the outer medulla [26]. NKCC2/BSC1 protein abundance is increased by water restriction, but the increase is less than in younger rats [22;26]. The decrease in NKCC2/BSC1 protein will reduce active NaCl reabsorption across the thick ascending limb of the loop of Henle, thereby reducing the generation of a hypertonic medulla and urine concentrating ability.

The protein abundances of the Ǝ and subunits of the epithelial sodium channel ENaC are also reduced [26]. Water restriction resulted in either no increase, or a reduced increase, in the protein abundances of ENaC, the sodium-protein exchanger 3 (NHE3), the Na+-Cl− cotransporter (NCC/TSC), and the sodium pump Na+-K+-ATPase [22;26]. Thus, the reduced maximal urine osmolality in aged rats may also be related, at least in part, to the reduced level of these sodium transporter proteins.


Urea Transporters
Urea is the second major solute that contributes to medullary interstitial hyperosmolality, and hence to urine concentrating ability [27-29]. Protein malnutrition reduces urine concentrating ability [30-34]. Elderly individuals may be at risk for protein malnutrition, especially those on fixed incomes. Two human (and two rat) urea transporter genes have been cloned: UT-A, which has 6 protein isoforms; and UT-B, which has 2 protein isoforms (reviewed in [6;8;9;35]). UT-A1 protein is expressed in the apical plasma membrane of the inner medullary collecting duct [36]. UT-A3 protein is expressed in the same segment of the collecting duct as UT-A1 [37]. Vasopressin increases urea permeability in the perfused terminal inner medullary collecting duct by increasing UT-A1 and UT-A3 phosphorylation and UT-A1 and UT-A3 accumulation in the apical plasma membrane [37-41]. Vasopressin phosphorylates UT-A1 at serines 486 and 499 [42]. The abundance of both UT-A1 and UT-A3 proteins is significantly reduced in 30 month-old vs. 10 month-old rats [21;43]; phosphorylation of serines 486 and 499 has not been studied to date (figure 3).


Urea transporters are reduced in 30 month-old rats compared to 10 month-old rats. Panel A: UT-A1 protein abundance. Panel B: UT-B protein abundance. Panel C: UT-A3 protein abundance. Asterisk indicates a significant difference between 30 and 10 month-old ...
Administering a supra-physiologic concentration of dDAVP increases UT-A1 protein abundance in the 30 month-old rats, but to a lesser degree than in the 10 month-old rats [25]. Inner medullary interstitial urea concentration is increased by water restricting the 30 month-old rats, but to a lesser degree than in the 10 month-old rats [43]. The reduced levels of UT-A1 and UT-A3 proteins will decrease urea reabsorption and inner medullary interstitial urea accumulation, thereby reducing the hyperosmolality of the inner medulla and urine concentrating ability. Thus, the reductions in UT-A1 and UT-A3 protein abundances, along with the reductions in AQP and sodium transporter protein abundances (discussed above), likely contribute to the reduced urine concentrating ability in the aged rats.

Glucocorticoids may be a mechanism that contributes to the decrease in UT-A1 abundance in aged rats. Older (30 month-old) rats have elevated plasma corticosterone levels as compared to 10 month-old rats [25]. Glucocorticoids decrease UT-A1 transcription, mRNA abundance, and protein abundance [44;45]. These findings suggest the hypothesis that increased glucocorticoids in aged rats may contribute to the reduction in UT-A1 protein.

UT-B protein is expressed on erythrocytes and in the descending vasa recta. A reduction in UT-B would reduce urine concentrating ability by reducing the efficiency of counter-current exchange and/or decreasing intra-renal urea recycling. People who lack the Kidd blood group antigen, which is also UT-B, and knock-out mice lacking UT-B, are unable to concentrate their urine to normal levels [46;47]. Thus, UT-B protein expression on erythrocytes and/or in the descending vasa recta is necessary to produce maximally concentrated urine [46;48-50].

UT-B protein abundance is significantly reduced in aged rats [21;43], and administration of supra-physiological amounts of dDAVP increases it [25]. Thus, another factor that may contribute to reduced urine concentrating ability in aged rats is the reduced level of UT-B protein.


Summary
Aged people and rats have a reduced ability to maximally concentrate their urine. Many of the key transport proteins that contribute to urine concentrating ability, namely AQP2, serine-256-phosphorylated AQP2, AQP3, NKCC2/BSC1, UT-A1, UT-B, and the V2-receptor, are reduced in the medulla of aged rats. The reductions in the abundances of proteins, and their reduced response to administration of a supra-physiologic dose of dDAVP or water restriction, contributes to the reduced ability of aged rats to concentrate their urine and conserve water. If similar mechanisms occur in human kidneys, it would provide a molecular explanation for the reduced concentrating ability in aging and may provide opportunities for novel therapeutic approaches to improve urine concentrating ability.


ACKNOWLEDGMENT
This work was supported by National Institutes of Health grants R01-DK41707 and P01-DK61521.


Footnotes
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Your Water requirements for daily life

How much should people drink? Official recommendations give guidelines for daily requirements.

The most recent official recommendation about water requirement has been published by the European Food Safety Authority in 2010.¹ This extensive scientific review has enabled the definition of adequate water intakes, based on European fluid intakes, desirable urine osmolarity and energy intake. The reference values assumed a moderate climate and moderate level of physical activity.

Table: Dietary Reference Values for water¹

 

These values include water that originates from both consumed fluids and food. The European Scientific Authority has also stated that the contribution of food to total water intake represents about 20% in adults. On this basis, it means that male adults should drink 2 L per day, and female adults 1.6 L.

No maximal tolerable intake level has been set by EFSA. This is justified by the great ability of healthy individuals to excrete excess water intakes within a large range of observed intakes. In healthy subjects the kidneys have the ability to excrete up to 0.7 to 1L/hour.¹

Reference

EFSA Panel on Dietetic Products, Nutrition, and Allergies (NDA); Scientific Opinion on Dietary reference values for water. EFSA Journal 2010; 8(3):1459. doi:10.2903/j.efsa.2010.1459. Available online:www.efsa.europa.eu.

TAPPING INTO THE BODY'S ENERGY

I have already mentioned the role of the human body's energy system in Thought Field Therapy (TFT). This program draws  upon Eastern tradition and its understanding of the presence and importance of energy in the human body. Let's look at the science behind it a little more closely.

  The Chinese use the term qi ( pronounced "chee") to describe the vital life energy. When the flow of this qi energy becomes blocked or imbalanced, according to the Chinese belief, it can trigger physical illnesses. Just as acupuncturists have developed ways to eliminate pain and promote physical healing by manipulating energy flow along a network of so-called meridians, or pathways, throughout the human body, It has been shown that these energy pathways can be accessed in order to heal emotional distress. 

  The human body's energy system has not been ignored by Western researchers, who have applied hard science to this ancient knowledge. As far back as the 1940s, Harold Saxon Burr of Yale University hypothesized that an internal energy system was key to human and all living things. Robert o. Becker, M.D., an orthopedic surgeon, used electromagnetic energy fields to stimulate the natural healing of broken bones and found that electromagnetic fields could be use to help regenerate amputated limbs in frogs. 

  Some of the most intriguing research was conducted by Dr. Bjorn Nordenstrom, a prominent Swedish scientist and radiologist and former president of the Nobel prize nominating committee. [ About Dr. Nordenstrom work, click here and here to watch youtube video]
In studies spanning two decades, he actually documented the existence of these electrical circuits in the human body. Dr. Bjorn Nordenstrom's interest in this area started when he observed a halo around malignant lung tumors and began looking for an explanation for this phenomenon. He identified a circulatory energy system in the human body, which he felt was just as significant to physical well-being as the blood circulation system. He demonstrated that electric circuits are carried by the interstitial spaces (the spaces between cells)and the blood vessels, and he believed that disruptions in the human energy system may play a role in the development of diseases as serious as cancer. He began cutting-edge research in which patients with metastatic cancer who were believed to be terminal were treated with applications of electrical currents -- with promising results. Another researcher, French biochemist Jacques Hauton, wrote that  Dr. Nordenstrom's findings led him to conclude that the electrical system"is not only as complex as the circulation of blood, but it also ....... intervenes in all physiology activity."

  In 1995, Pierre de Vernejoul provided concrete evidence that the meridian network does exist. He and his team of investigators injected non-harmful radioactive technetium 99m into the arms and legs of human volunteers at the sits of commonly used acupuncuture points along the meridian system. Then they used gamma-camera imaging to track the flow of this injected material. They found that the radioactive isotope traveled specifically along the meridian pathways that the Chinese had identified thousands of years ago. By contrast, when the substance was injected randomly elsewhere in the human body, it did not move along any specific internal pathway. The bottom line: The meridian system is an actual, clearly defined network -- the same one the Chinese have been using for millennia. 

  Thus, the energy system used in Thought Field Therapy is genuine, not some mystical notion. Every perturbation in the Thought Field is associated with a specific energy meridian. My own research has shown that the meridian system is a governing force in controlling and healing the disturbing emotions. Best of all, this system can be accessed by TFT. This is true whether the psychological problem is anxiety, trauma, addictions, panic attacks, phobias, anxiety, anger, jealousy, or depression. More recently, we've learned that TFT seems capable of producing physical healing as well. By tapping on specific points along the human body's energy meridians, re-balancing and healing can take place at the most fundamental level, weakening and eliminating the underlying negative emotion or physical ailment. AS the stimulation from this tapping influences the internal electromagnetic energy, it has a direct effect on the Thought Field and the perturbation associated with the problem being treated. 

  As you learnt he self-administered algorithms that are key to Thought Field Therapy, you will tap on points along these energy meridian that have been chosen specifically for the particular emotional (or physical) distress you're having, and sequenced in a specific way, like the order of a combination lock. If the sequence is wrong or the points are inappropriate, the lock won't open; but if they are correct sequenced and tapped, healing will occur, rapidly and usually permanently. The "recipe" for each problem has been initially validated on hundreds and, in some cases, even thousands of people and is now widely accepted and used as an algorithm. Each can achieve predictable results in patient after patient. 

THE ANATOMICAL REALITY OF ACUPUNCTURE CHANNELS: CONNECTIVE TISSUE? 

Posted on January 13, 2013 by Boyd Bailey, L.Ac.

Way back in 1992, 3 French guys submitted a paper to a prominent acupuncture journal detailing a unique experiment.  They injected 250 healthy folks and 80 with kidney disease with a radioactive tracer at a common acupuncture point on the inner ankle associated with kidney function (Kidney-7) and used a gamma camera to track its migration.

Low and behold the techetium-99m (99mTc) flowed exactly along the traditionally known Kidney Channel in both groups. Apparently they ruled out the possibility that this migration, this flow of the radioactive isotope was either vascular or lymphatic, but rather along connective tissue planes.

This would seem a groundbreaking discovery, and so my question for you, dear reader- especially y’all in the field – is WHY we’ve not heard more about this, why similar studies have not been performed, why the lack of follow-up? Or perhaps there has been… In which case please enlighten me!

A Study on the Migration of Radioactive Tracers after Injection at Acupoints

Objective: This paper reports on the authors’ investigation of the pathways of acupuncture meridians in the human body through the injection of radioactive tracers (isotopes) at acupuncture points.

Design: The radioactive tracer used was the most common radioactive tracer, techetium-99m (99mTc), as sodium pertechnetate. The experiment was conducted with a gamma camera, a Siemens SAM (small-area mobile) digital scintillation camera. Image analysis was conducted by a computer system built into the camera. Morphological studies and quantitative dynamic studies were conducted.

The morphological studies consisted of analytical and differential studies. For the analytical studies, the radioactive tracer is injected at a control point located outside any acupoint. Then, another injection is given at an acupoint.

The differential analysis was conducted in order to establish the specific and unique characteristics of the pathways observed in the analytical studies and thus eliminate a vascular or lymphatic explanation. To investigate the vascular pathways, two radiotracers of different energies and therefore discernible by spectrometry were utilised: Technetium-99m was injected as an acupoint and Thallium (201TI) was injected in a small vein situated next to that acupoint. To study the possible relationship between the lymphatic pathways and those demonstrated by the radiotracer, the same dose (20 MBq) and volume (0.05ml) of pertechnetate was simultaneously injected at an acupoint and the first interdigital space of the foot. A quantitative study of the previous data was conducted after selecting two mirror regions of identical shape and size on the leg along the Liver meridian (an acupuncture meridian) and similar “background noise regions” outside the pathways.

Sequential study and stimulation studies were conducted as part of quantitative dynamic studies. The goal of the sequential study was to evaluate the speed of radiotracer migration along preferential pathways. In healthy control subjects and patients with unilateral renal pathology, two sodium pertechnetate injections of identical volume and activity were given simultaneously at the left and fight acupoints K-7. In the stimulation study, mechanical, electrical, and thermal stimulation were performed on certain acupoints after the injection of radiotracers to study the migration of the radiotracers.

Laboratory experiments conducted in collaboration with the Cytology Laboratory of the Military Hospital of Percy in Paris tested modifications of granulocyte membrane potentials during stimulation of an acupoint using either a needle or a laser beam. The cell membrane potential was measured with a fluorometric method on blood sampled one minute after the end of injections or stimulation’s, and compared with control blood from the same subject.

Setting: The work was conducted on patients from the Department of Urology and from the Acupuncture Department of Biophysics and Nuclear Medicine from the Necker Hospital in Paris. Each experiment was repeated several times.

Patients and Other Participants: The work was conducted on over 250 healthy control subjects and on 80 patients with renal pathology.

Main Outcome Measures: The authors expected to find that the preferential pathways taken by the radiotracers coincide with the acupuncture meridians as described in Chinese traditional medicine and that these pathways are distinguishable from either lymphatic or vascular mutes.

Results: Morphological studies found those tracer migrations from acupoints in both healthy and sick patients followed the same identical pathways with those described as “meridians” in Chinese traditional medicine. The results suggest that these pathways are different from vascular and lymphatic pathways.

The quantitative dynamic studies found that in injections at bilateral K-7, there was a faster diffusion on the healthy side, and slower diffusion on the diseased side. In inflammatory organ disease, there was increased migration speed of the radiotracer in the meridian of the related organ. A reduced tracer migration speed is indicative of a degenerative disease, such as cancer. Such findings could be used as the basis of a therapeutic evaluation or diagnosis. The laboratory experiments with cell membranes suggests that acupoint stimulation could be used to provoke constant and reproducible change in cellular physiology.

Conclusion: The migration speed and patterns of a radioactive tracer along pathways which coincide with the Chinese acupuncture meridians show that these routes have neither a vascular nor a LYMPHATIC origin. These pathways are very likely related to the connective tissue diffusion following the neurovascular bundles along the extremities. Findings suggest the hypothesis of the intervention of a neurochemical mechanism in information transmission.”

American Journal of Acupuncture, Vol. 20, No. 3, 1992

Writers: Jean-Claude Darras, Pierre de Vernejoul, and Pierre Albarhde; C.H.U. Necker – Enfants Malades, F-75 743 Paris Cedex 15, France.

Urine Bubbly?

What does it mean when you have bubbles in your urine?
The presence of bubbles in urine or foamy urine is a common clinical symptom hinting at proteinuria in kidney failure patients. But urine with bubbles does not necessarily mean that you are suffering from kidney disease. Bubbly urine can be due to a relatively benign or harmless condition as well. Proteinuria is the presence of excess proteins in the urine. In healthy persons, urine contains very little protein; an excess is suggestive of illness. Excess protein in the urine often causes the urine to become foamy, although foamy urine may also be caused by bilirubin in the urine (bilirubinuria),retrograde ejaculation, pneumaturia (air bubbles in the urine) due to a fistula, or drugs such as pyridium.

What does it mean when your pee is foamy?

A full bladder can make your urine stream faster and more forceful, which can cause foam. The urine can also get foamy if it's more concentrated, which can occur due to dehydration or pregnancy. Sometimes, the problem is your toilet. ... Protein in the urine is another cause, and it's usually due to kidney disease.

What does it mean if you have foam in your urine?

This can be a sign of protein in your urine (proteinuria), which requires further evaluation. Increased amounts of protein in urine may indicate a serious kidney problem. If your urine seems unusually foamy most of the time, your doctor may recommend that your urine be checked for elevated levels of protein.

Why does my pee smell so strong?

Consumption of certain foods, such as asparagus (which can impart a characteristic odor to urine), and taking some medications may be causes for changes in the odor of urine. The presence of bacteria in the urine, such as with a urinary tract infection (UTI), can affect the appearance and smell of urine.

What does it mean if you have protein in your urine?

Protein in urine (proteinuria) Protein in the urine, also called proteinuria, is often a sign of kidney problems, or an overproduction of proteins by the body. Healthy kidneys only pass a small amount of protein through their filters.

How much is too much protein in the urine?
Here are some natural home remedies that can aid in treating proteinuria:

1.Eat plenty of fruits and vegetables, grains, and legumes.
2.Lean meats are better than red meat, as the latter is harder to break down.
3.Consume more fish.
4.Restrict salt intake.
5.Drink plenty of water and avoid soda/caffeine/coffee.

6.Exercise regularly.

Why would you have protein in your urine?

Both diabetes and high blood pressure can cause damage to the kidneys, which leads to proteinuria. Other types of kidney disease unrelated to diabetes or high blood pressure can also cause protein to leak into the urine. Examples of other causes include: Medications.

How do you get rid of protein in the urine?
1.Keep track of the amount of protein you are eating. ...
2.Help your kidneys flush out and remove excess proteins from your body by drinking plenty of extra water. ...
3.Make a permanent commitment to change your reduced protein diet. ...

4.Focus your diet on foods which are natural and lower in protein.

What does it mean when your urine is cloudy?

Cloudy urine can be caused by a variety of conditions, including vaginal discharge, sexually transmitted diseases, dehydration, certain autoimmune disorders, as well as infection, inflammation, or other conditions of the urinary tract (kidneys, ureters, bladder and urethra).

What are the main causes of kidney stones?

Kidney stones form when your urine contains more crystal-forming substances — such as calcium, oxalate and uric acid — than the fluid in your urine can dilute. At the same time, your urine may lack substances that prevent crystals from sticking together, creating an ideal environment for kidney stones to form.

What can cause your urine to smell?

Some foods and medications, such as asparagus or certain vitamins, can cause a noticeable urine odor, even in low concentrations. Sometimes, unusual urine odor indicates a medical condition or disease, such as: Bladder infection. Cystitis (bladder inflammation).

Why does my pee smell like ammonia?

Eating foods rich in protein can cause this smell, especially if you eat a lot of them. That's because the foods can lead to excess nitrogen in your body, and when that is released, it smells like ammonia. Dehydration. If you don't have enough water in your body, your urine becomes very concentrated.

Can proteinuria be cured completely?

In such cases, proteinuria is temporary and it can be completely reversed after the underlying cause is eliminated. However if proteinuria is caused by chronic kidney disease, diabetes or hypertension. ... Proteinuria is typical symptom of kidney disease which is one of the major causes of protein leakage in urine.

Proof that an oral saline IV is better than a USD$525.00 intravenous one.

Oral vs IV Rehydration

Athletes Take Heed

When considering oral vs IV rehydration, oral is better. Why? Here you will discover what we think, what we know and what can we prove.

Both oral and IV hydration have been used by high-performance athletes through the years. It is common in the NFL, collegiate football, marathon and triathlon sports.

In third world and some second world countries, IV rehydration for athletes is a standard of care.

One Size Does Not Fit All

Research from 2005 found oral re-hydration to be more effective in children than IV fluid (IVF) rehydration, because it was faster to give and reduced hospital admissions in a certain group of small children.

When someone is unconscious or semiconscious, IV administration is the preferred form of hydration by healthcare professionals. But what about the rest of us? Is there a better way?

Oral vs IV Rehydration: The Sport Health Pro View

Because of the commonality of IV use, health professionals believe it is more effective than oral rehydration. It is thought that the IV will provide for far greater performance over oral hydration.

However, this is wishful thinking. There is no science to back this mindset.

Benefits Of Oral Hydration: The Science

Oral hydration has been found to be just as effective as IV hydration and studies show that oral hydration may actually be more beneficial. Oral hydration is also safer. It does not require medical staff to deliver it.
The safety and speed of administration alone makes it a better choice on the field of sports activity.

The study looked at the response to IV and Oral Rehydration. After 20 minutes of rehydration, the subjects exercised untill exhausted. The room temperature was 98.6 degrees Fahrenheit with a humidity of 50%.

The findings....

During exercise, the....

Blood plasma (the liquid part of our blood) and other blood-pumping values were about the same for IV and oral rehydration.

Temperatures were lower with oral rehydration.

Feeling of thirst was lower in the oral rehydration group.

Feelings of exertion were lower in the oral rehydration group.

Performance improvement for the oral rehydration group were only slightly better.

Oral Rehydration: The Better Way

While the results were about the same in the IV vs Oral hydration methods, there are a number of unseen advantages. The risk of infection, bruising, discomfort may be considered minor reasons to avoid the IV. Any invasive treatment to the body has greater risks than natural treatments.

Additionally, the need to move an athlete to a secure place to provide the IV creates further challenges.

Add to this the thirst perception and the feeling of not being exhausted, the oral rehydration has a lot of reasons to consider it as being superior.

By following an effective oral rehydration protocol, athletes are taking charge of their own health naturally. This will help the athlete become more in tune to their body's needs and when it is speaking to them. This in turn may result in greater performance.

So, when it comes to oral vs IV rehydration, oral wins the competition.

Research

Intravenous vs. oral rehydration: effects on subsequent exercise-heat stress.
J Appl Physiol (1985). 1997 Mar;82(3):799-806

Thermoregulation and Stress Hormone Recovery After Exercise Dehydration: Comparison of Re-hydration Methods
J Athl Train. 2013 Nov-Dec; 48(6): 725–733

A related trial in young children, even better results.

Oral versus intravenous rehydration of moderately dehydrated children: a randomized, controlled trial.

Pediatrics. 2005 Feb;115(2):295-301

So, How Much Water To Drink?

The following is the baseline water needs.

Age 2-17y-o daily minimum need is 75% body weight in ounces of water. Divide by 5 or individual dose. Take a pinch of salt dissolved on the tip of the tongue each time you drink.

Age 18+ daily minimum need is half the body weight in ounces of water. Divide by 5 or individual dose. An easier way, 10% your body weight each time you drink. Start with 2x and work up to 5 times. Take a pinch of salt dissolved on the tip of the tongue each time you drink.

Here is the break down and those who should not use this. Please read this entire section to find your specific need.

NEVER: drink more than 32 ounces in 2 hours.

NEVER: drink the water without taking the salt (unless otherwise directed). Too much water could wash out the electrolytes needed for normal health.

NEVER: Use the protocol if you have kidney disease without talking to a doctor.

NEVER: Use the protocol if you have congestive heart disease (CHF) or other fluid restrictions.

NEVER: use the protocol if you have a salt intolerance.

The Five Rights of Proper Hydration

Right Person: age 2-17 / 18-50 / 50-80 / 80 and older.

Right Time: 30 min before and 2 hours after meals.

Right Route: Dissolve the salt in mouth so it can be absorbed in the mucous membranes.

Right Amount: Salt: 1/8th tsp per 16 ounces, water: 10% of body weight in ounces of water each time you drink.

Why Dissolve the Salt On the Tip Of Your Tongue?

Some drink water with salt in it. This is called Sole. It can and will make many people sick to their stomachs. Putting the salt on the tongue will allow it to get to the blood faster so that when the water arrives in the gut, it will better be able to be absorbed.

Right Electrolyte: While normally this would be unprocessed salt, it could include others depending on your health issues.

Right Person Age 2-17: If there are any health problems, do not use the water cures protocol without supervision of a healthcare provider. The growing years...According to Dr. B, the formula is 75% of their body weight in ounces of water is the total daily dose. Then divide by 5 or 6 for individual dose. During athletic performance, the hydration need goes up to 100% of their body weight in ounces of water.

Right Person Age 18-50: Start drinking the water 2 x a day (within 20 min of waking) and slowly increase.

Right Person Age 50-80: Start off slower. Use the least amount of water and the least amount of salt. Only start off drinking one time a day. Then after a week, increase to 2 times a day. Allow up to 30 days before increasing the amount of water you drink or the salt you take.

Right Person Age 80 and over: Only start with the help of a healthcare professional. You should be monitored for health changes.

Right Person 18-50: If you do not have any other health issues, this age group usually responds to the basic water cures protocol.

Right Route: Obviously you are going to drink the water. The electrolytes are another story. Some prefer putting salt in the water. This may make you sick to your stomach. Others prefer putting the salt on the tongue and letting it dissolve. There is a third way that also makes sense.

When adding a tablespoon of liquid chlorophyll to the last drink of the day, adding level teaspoon of honey and 1/4 tsp of salt into the glass, blend into the water, and it will be more easily absorbed in both your mouth before swallowing and in your gut after it goes down.

Note: By using the oral route, the best way to make it most effective, hold each sip in the mouth and allow your saliva to mix with it as well as some of it to be absorbed.

Right Amount: This is broken down into four answers. There are individual doses, daily doses and doses for those highly active or in very hot or humid conditions.

Drink the water all at once. Do not nurse your water. Think of your body as holding it rather than holding it in a bottle. The salt is what allows your body to store it.

One thing to note, many start losing weight. Sometimes the weight loss is dramatic. The amount of water we need will gradually decrease as you follow the water cures protocol.

First: Never drink more than 32 ounces at one time or inside of a 2-hour period and never drink that much without salt.

Individual dose: At a normal activity level, 10 percent of your body weight in ounces of water. So If you weigh 135 lbs, you would drink 13 ounces. If you weigh 190 lbs, you would drink 19 ounces. Ten percent in ounces is basically the first two numbers of your weight if you are over 100 lbs and the first number if you are under 100 lbs.

This is the baseline amount you need to drink. If you are active, you will need to drink more depending on the intensity of what you are doing.

There is science on drinking more. Urine Volume and Change in Estimated GFR in a Community-Based Cohort Study. Conclusions in this community-based cohort, decline in kidney function was significantly slower in those with higher versus lower urine volume.

Right Time: 30 to 45 min before meals, 2 hours after meals. The reason is simple. When we drink water and take the electrolytes on an empty stomach, the water more readily goes through the stomach and enters the gut. From there, it returns to the stomach through the blood circulatory system and prepares the stomach for the soon-to-arrive food. The preparation includes both having everything ready for the production of hydrochloric acid and the creation of the mucous lining for the arrival of the food. Additionally, any old salts are washed out of the stomach.

In addition to being the best practice of hydration of the body and to avoid diluting the stomach juices, drinking before allows the stomach to better prepare for the meal.

If you are doing water to lose weight, drink as soon as you get up. Ideally you want to drink your water and dissolve the salt in your mouth within 20 minutes of awaking. Likewise drink at least 20 minutes before bed.

Right Electrolyte: Normally the Water Cures protocol suggests using unprocessed salt. However, there are exceptions. While we do not understand the reason why, some fine ground sea salts tend to have less mineral counts than the coarse salts. This may be due to oxidation from exposure to air. So we recommend the coarse sea salt as perhaps the best.

And not all sea salt has the same mineral counts. It must be unprocessed. The best way to know, look for the mineral count. Mined salts likewise are rich in minerals. Some prefer one over the other. The best way to find out which works best for you is to try both or even switch back and forth.

Sometimes we may need additional electrolytes. Your doctor would be in the best position to tell you if you should use any others, how much and how long.

How Much Water to Drink to Prevent Dehydration
This is a work in progress. We will continue to study and define the answer to this question. One thing we do know, when there is illness or disease, the water cures protocol can help some to reset their health.

Please share your experience or questions to help us grow this knowledge base.