With the focus of exercise usually on metabolism and performance of muscles, the effects of physical exertion on other organs might be forgoten. The kidney plays critical roles in maintaining hydration and electrolyte balance, removing waste, and regulating acid-base balance.

THE KIDNEY'S ROLE

The kidneys play a pivotal and essential role in maintaining hydration of the body, or body fluid homeostasis. If the body is in a situation where a fluid deficit exists (e.g. dehydrated state), there will be a compensatory decrease in the production of urine and the small amount of urine produced will be extremely concentrated; it will appear very yellow in color. If fluid intake is excessive or if the body is overly hydrated, the kidneys attempt to correct this situation by increasing the production of urine; the urine will be very dilute and clear in color.
Urine output for a normal adult dog usually ranges from 0,8 to 1,8 liters per day. This filtration volume is needed to deliver large amounts of metabolic by-products and toxins to the urine for elimination from the body. More than 99% of this filtrate is reabsorbed by increased water and salt reabsorption in the proximal and distal segments of the nephrons; pure water is reabsorbed in the collecting ducts of the nephrons as well. The effect in the proximal tubules is related to glomerular blood flow; that in the distal tubule occurs via the action of aldosterone, a hormone generated from the adrenal glands in response to water and salt depletion. The effect in the collecting ducts occurs via the action of anti-diuretic hormone (vasopressin), a hormone released by the brain in response to decreased volume of fluid in the heart and/or increased concentration of solutes in extracellular body fluids.

THE KIDNEY FUNCTION IS CHANGEING DURING EXERCISE

Exercise produces changes in renal hemodynamics with alterations in electrolyte and protein excretion. Effective renal blood flow seems to be reduced relative to the intensity of exercise such that renal blood flow decreases with increasing intensity of exercise. This is the result of the shunting of blood away from the renal and splanchnic vascular beds to exercising muscles. Renal blood flow relative to cardiac output may be quite low during exercise, but the absolute flow really is quite consistent at rest or exercise.
In the case of vigorous exercise accompanied by large fluid losses, increased water and salt reabsorption occurs in the proximal and distal tubules. The additional water reabsorption in the collecting ducts is related to elevated levels of anti-diuretic hormone in the blood. The water and salt reabsorbed from the urinary filtrate is returned to the blood vessels.
Although this conservation of body water and electrolytes is beneficial for an athlete, there is a misconception about its importance. Because urine production at rest is relatively low , the maximum amount of water that could be conserved by the kidneys during exercise is of little consequence. The kidneys' real importance is during the 24-48 hour period after exercise, in terms of recovery from a dehydrated state and the restoration of body fluids.

DEHYDRATION HURTS THE KIDNEY

Severe dehydration associated with low blood volume will cause poor renal blood supply and poor renal delivery of oxygen and glucose, especially to the renal tubular cells. If a critical level of supply is not maintained to these cells, injury occurs to the cell membranes and energy sources inside the tubular cells are depleted.
The resultant clinical condition, acute tubular necrosis, occurs only with severe acute fluid losses (eg., hemorrhage) or severe dehydration ( acute loss of 15% or more of body weight in fluids), and can lead to the inability to excrete waste products, electrolyte disturbances and acute renal failure. This condition may be self-limited with recovery in days to weeks or may lead to permanent renal damage.
With the levels of dehydration typically seen in athletes under stresfull conditions, generally in the range of 5-8%, we don't know if there are any permanent ill effects of dehydration on the kidney. The possibility of negative consequences was first raised by studies examining the urinary profiles of dehydrated dogs. The findings showed the excretion of leucine amino peptidase, an enzyme that may indicate kidney damage.

 KIDNEY STONE AND DEHYDRATION

Kidney stones, or renal calculi, are crystalline structures that typically contain phosphate or calcium oxalate as the sole or major component. There is no single explanation of the cause and development of stones. In all probability, stones result from the interaction of multiple factors. It is generally thought that a period of abnormal crystalluria is required during which large crystals, or aggregates, are produced in the urine. In order for these crystals to continue to grow, a certain number of chemical factors must be present - i.e., the urine must be supersaturated with the salt of the stone-forming crystal; certain inhibitory factors of crystallization must be reduced or absent from the urine; and the environment in the urine must be conducive to the aggregation of the crystals.
Kidney stones may form in the kidney, in the ureter draining the urine from the kidney, or in the bladder in susceptible individuals. This usually occurs secondary to a urinary tract infection or in individuals who have high urinary calcium excretion, a condition that is most commonly seen in relation to excessive calcium and/or vitamin D intake.
The most likely candidates for a kidney stone are the dogs with diets high in oxalate or from excessive vitamin C intake, or high uric acid excretion, or related to high protein intake, may lead to stone formation.
Males are more likely to form stones because they have more calcium and uric acid in their urine, and because they are worked  in the heat and become dehydrated. It is dehydration, not exercise - that increases the risk of stone formation.
Recent studies finds that individuals who eat the most calcium have the lowest risk of stones. Because calcium binds oxalate in the gut, so it passes in the stool and does not enter the body. Sodium  is not a key risk for renal stones, yet cutting sodium can lower the risk of stones. This is because sodium and calcium seem to compete for absorption by renal tubules. So the less sodium you eat, the less calcium stays in the urine.
Nevertheless, sodium-induced calcium stones in susceptible individuals probably occur as a result of chronic exposure to sodium. Very prolonged intake of excess sodium would be required to develop the high urine sodium excretion that apparently contributes to this condition.
The dehydration resulting from exercise increases the concentration of calcium and oxalate in the urine. In normal individuals, the conditions are not such that this results in formation of kidney stones. In individuals with defects in calcium and/or oxalate excretion, the conditions of hypercalcuria and/or high excretion of oxalate plus dehydration may cause problems.
 The most critical tip to preventing stones is to quaff fluids -one or more liters per day - to keep the urine dilute. Other dietary tips include eating more potassium (which somehow lowers urinary calcium excretion), cutting oxalate-rich foods , avoiding large doses of vitamin C, and reducing animal protein in the diet.

THE KIDNEYS REGULATE THE LEVELS OF SODIUM AND OTHER ELECTROLYTES IN THE BODY

The kidneys help maintain normal body levels of sodium and other electrolytes by urinary retention and/or excretion of these electrolytes. Sodium and chloride are the major extracellular electrolytes. The level of these two ions in the extracellular fluid compartment must be kept in a relatively narrow normal range for proper body function. Sodium and chloride are freely filtered into the urinary filtrate in the glomeruli, and reabsorption in the proximal and distal tubules occurs based on renal blood supply, circulating blood volume and electrolyte levels. If blood volume is low, as occurs with hemorrhage or dehydration, sodium and chloride reabsorption is increased and water is reabsorbed with these solutes. In the event of total body depletion of sodium and/or chloride, blood volume is often low as well since vascular volume is dependent on adequate solutes in the blood. In this case, sodium and chloride reabsorption with water is again maximized in the kidney. Under appropriate conditions, like dehydration or salt depletion, urinary levels of sodium and chloride are quite low. Even though urine flow and salt excretion can be dramatically curtailed under appropriate conditions, it can never be diminished to zero.
Conversely, the kidneys can dump huge amounts of sodium to compensate for a high sodium intake. Sodium in general does not stress kidneys, but controversy exists on sodium and blood pressure. Sharply cutting salt can lower blood pressure. Surely most athletes, who lose sodium, need to restore it in a sports drink, for example.

HIGH PROTEIN DIETS  AND ITS EFFECT ON THE KIDNEY

High dietary protein or amino acids accelerate the progression of renal disease. A key issue is that amino acids are renal vasodilators. As such, they decrease pre-glomerular vascular resistance, thereby exposing the glomerular capillary to a greater-than-normal hydrostatic pressure. The resultant "glomerular hypertension" causes glomerulosclerosis and damage to the nephron.
Based upon what we currently know, I feel it is appropriate to caution trainers that excessive amino acid or protein dietary intake on a chronic basis could damage the kidney by elevating glomerular capillary pressure and causing glomerulosclerosis. This deleterious effect may increase the possibility of renal disease later in life.
A low-protein diet can help prevent glomerular hypertension and thus slow glomerular sclerosis in residual healthy nephrons.
A high protein diet, with its load of urea, phosphate, sulfate, urate, and hydrogen ions, raises glomerular filtration rate, whereas a low protein diet lowers it. But in healthy dogs, this has no demonstrable consequence.

EXERCISE-RELATED ACUTE RENAL FAILURE

This is an uncommon syndrome of oliguria or anuria with renal (mostly "tubular") dysfunction that usually occurs during long show when the physiologic decrease in renal blood flow is augmented by blood loss, heat stress, dehydration, and exertional rhabdomyolysis (the breakdown of skeletal muscle). It also occurs and can kill via hyperkalemic cardiac arrhythmias. Risk factors include low fitness, unwise exertion, and poor hydration.
Fortunately, exercise induced acute renal failure is rare. For reasons which are unclear, adequate glomerular filtration is maintained at normal levels, despite intense neurally mediated renal vasoconstriction during exercise.
Rhabdomyolysis is a key event, in association with exercise, that may precipitate acute renal failure. Rhabdomyolysis is most likely to occur in situations that include one or more of the following: prolonged intense exercise, heat stress, dehydration, and potassium depletion. There are, however, reports of rhabdomyolysis and renal failure occurring in untrained subjects following short term maximal exercise.
Preceding infectious processes, especially vital, may predispose one to muscular injury that could precipitate rhabdomyolysis. This may be exacerbated by use of analgesics (aspirin and non-steroidal anti-inflammatory agents) for minor injuries. These drugs inhibit the renal vasodilatory prostaglandin production. Therefore, an important compensatory mechanism for the physiologic decrease in renal blood flow is impaired. This effect increases the risk for renal ischemia. Myoglobinuria, hemoglobin-uria and nephrotoxic drugs may intensify the physiologic renal response to exercise. This, in combination with volume depletion, leads to renal ischemia and acute renal failure.
In this situation, the cornerstone of management is early and aggressive fluid replacement. Urine output should be closely monitored and if the dog is oliguric for more than a few hours, hospitalization may be necessary for intravenous volume expansion and observation.

CONCLUSIONS

The kidney serves a critical role in helping to maintain normal homeostasis (fluid and electrolyte balance) during, and more importantly after exercise. The effects of exercise  on the kidney are unclear. More than likely, exercise has large indirect effects on acute kidney function via altered blow flow and possible dehydration.
The biggest problem in dogs mortality is the renal failure. Renal failure can appear by age or after a sustained effort. Exercising the kidneys like all the other parts of his body is an important thing.
But how can we exercise the Kidneys? The answer is by making them work during feeding and training.
During the hard trainings the kidneys are playing an important work by filtering the residues and also by maintaining an equilibrium in the hydro-electrolytic balance.
During feeding, if you feed them liquid meals the excess liquid will be eliminated trough the kidneys, making them work. The excess liquid in the feed makes the kidneys filter more easy the residue in the body. The residues are usually eliminated trough fecales and urine. If the urine is concentrated with residues then each time they will pass the urinary system they will affect the glomerules of the kidney and in time can lead to renal failure.
These are only some general guidlines that all of us know but you always have to remember that each dog is an individual and we have to adapt to their needs.