Gout, Renal Impactions, Nephritis, Uremia

The kidneys of birds have the particular property of being able to deal with richly nitrogenous waste material and concentrate the watery fluid which filters through the renal glomeruli, so that the "urine" is semi-solid on excretion. Specific infections of the kidney are uncommon, but bacteria are sometimes present, either as the result of a septicaemia or by direct spread from an adjacent diseased organ such as the intestine or reproductive tract. Another common problem with the urinary system is Clagged Vent or Pasting of the Vent. A bird has two reddish-brown kidneys, each consisting of three lobes. They are set into cavities in the heavy pelvic structure, one on each side of the spine. Each kidney is drained by a ureter running along its ventral (towards the front) surface and emptying into the cloaca. The fragility and sensitiveness of a birds kidneys is well illustrated by the protection nature has afforded them. The bony structure encasing them on all but the ventral side is the strongest of the entire skeleton, not exceeding the skull. Two main problems with the kidneys cause yellow kidneys (Nephritis) or gray kidneys (Uremia).


Articular & Peri-articular Gout on feet of Budgerigar
It may seem strange that birds are prone to this disease which is traditionally associated with the well-to-do of bygone days who were given to consuming inordinate quantities of venison and claret! Gout is due to failure to eliminate nitrogenous waste products from the bloodstream through the kidneys. As a result, insoluble material, mainly in the form of urates and related substances is deposited in certain areas of the body. In birds, an excessive appetite, especially for an unbalanced diet, combined with inactivity, are undoubtedly predisposing causes. Renal disease of different kinds including nephritis (inflammation of the kidneys) can produce gout. Two types of gout occur in birds, named according to the distribution of the lesions: articular and visceral gout. They are most frequently seen in gallinaceous birds, budgerigars and waterfowl, to a lesser extent in parrots, and less frequently in pigeons and canaries. Sporadic cases or even outbreaks of gout can occur in many species. In articular gout, which is much less common than the visceral form, urates are deposited around the joints, the tendons sheaths, tendons, ligaments and periosteum. Accumulations of these deposits produce cream-coloured, shiny swellings which bulge up through the overlying skin and subcutaneous tissues. The swellings seem to be intensely painful especially when the affected joint is touched or manipulated. The lesions may distort and cripple the limb. If a swelling is incised, the contents are found to be of a creamy, pasty or gritty consistency, according to the amount of fluid accompanying the urates. The creamy and pasty types may easily be mistaken for abscesses, though in fact they rarely take this form. In the early stages, gout is easily mistaken for a type of acute, infective arthritis. Visceral gout is more insidious and lethal than the articular type, although probably less painful. The two types often coexist. In visceral gout the deposits are to be found in almost any organ of the body cavity, but the liver, kidney, pericardium, heart and air sacs are most frequently affected. Beige, white, or occasionally, pale, yellowish deposits are seen on the peritoneal or serous surfaces of the organs. Sometimes the deposits infiltrate into the organs themselves and a few important diseases may be confused with this form of gout, such as aspergillosis or other infections affecting particularly the abdominal or thoracic air sacs. Egg peritonitis may give rise to similar lesions, but the deposits of yolk can more easily be scraped off the surfaces of the organs and they are more yellow in colour.

Gout has long been associated with overeating, especially of protein foods, but it also occurs as a result of malnutrition. The "Poor man's gout" of past ages was a scourge of people on the breadline who also drank a large amount of alcohol. In such cases there was doubtless a protein deficiency. Instead of an otherwise healthy liver and kidney overworked and damaged by excessive metabolism of rich food, these organs are striving to function by converting a low-protein, low-vitamin and high-carbohydrate diet into utilisable body substances, while their mechanisms are badly impaired by dietary deficiencies. This may explain why in birds, a low diet, even more than one high in protein may result in nephrosis (kidney disease) and gout. As an example the author can recall a female budgerigar kept by a schoolmistress for her children, which bred over 20 offspring in two seasons on a diet of only 80 per cent millet, 20 per cent canary seed, plus a little grit. At 13 years of age it was a lean but still lively bird, with large gouty swellings affecting both hocks and feet. The teacher, however, was very careful to follow instructions about diet, and the bird recovered in about six weeks. It remained clinically normal for at least a further two years, when it received treatment again for quite a different reason. Treatment depends upon establishing whether the gout is due to overeating, a high-protein or low-protein diet, or if there is an amino acid or vitamin deficiency or imbalance in the diet. The fact that so few birds respond well to dietary adjustments is probably mainly due to the fact that the kidneys have become permanently damaged, and partly due to the inability of many people to persevere with a new diet for several weeks, when this at first is usually rejected by the bird leading to initial loss of weight. Having assessed the protein intake, it can be increased by adding egg, grubs or insects, or reduced by adding cereal products to the diet. At the same time, a mineral and vitamin supplement must also be given. A caged bird should be put into a flight or planted aviary if at all possible, because muscular activity stimulates the circulation and the thirst, both of which should help in the dispersal and excretion of urates. Water intake can also be increased by placing a pinch of salt in the drinking water. Green food and fresh fruit should also be given. With many species perseverance is necessary to ensure that the bird eats a satisfactory diet.

Birds have no urinary bladder, and urine is temporarily held in the cloaca. The flow of urine down the ureters is normally almost continuous. Sometimes, however, it may be interrupted; for example, when there is excessive water reabsorption in the kidneys, as may occur when drinking water is not available. The urine then becomes thickened or pasty and it is only slowly excreted. If it is withheld too long, irreparable damage occurs in the kidney, waste products build up in the bloodstream and rapidly poison the bird. When sudden deaths occur with little or no previous signs of illness, these accumulations of solid, pasty, urate material are often found in the kidney tubules or ureters. Normal urine in these structures is of a translucent watery consistency.

Please consult a vet before using any medicines mentioned in this article below as it was written some time ago and new ones should be available with better results.
Kidney disease (nephrosis) including inflammation of the kidneys (nephritis) may be due to irritation of the glomeruli, tubules or ureters by infection or toxic substances, including over stimulation by certain drugs. These may be an alteration of the rate of filtration, reabsorption or ureteral flow of urine during its production. Increased blood flow to the kidneys increases the rate of filtration. According to the cause, this may be followed by increased or decreased reabsorption of water, salts, sugar and other useful commodities. The same causes may produce swelling of the lining membranes of the tubules and ureters, interfering with the absorption and flow of fluid respectively. At post-mortem examination especially following sudden death, these sort of lesions are quite frequently found, and are associated with congestion of the kidneys and with no other significant disorders. Whether the primary cause is due to a virus, a poison, allergy, chilling or shock can seldom be established, even after exhaustive laboratory tests which may take several weeks to perform.

Nephritis, as the name indicates, is any inflammation of the kidneys. The type of nephritis to which birds are commonly susceptible is identical with Bright's disease in man, a chronic fatty degeneration of one or both kidneys. This condition is not described in any literature on birds to come to my attention. It is hard to believe that a condition so common could escape observation, but that is evidently the case, since all books describing the symptoms of this condition attribute those symptoms to other pathological changes which, by the way, do not occur under the circumstances described as contributing causes. I have observed this condition in canaries, finches, sparrows and blackbirds and have reasons for believing it to be of common occurrence in all species of birds, both wild and domesticated. The only reason I can see for this condition escaping observation is the fact that most bird keepers are too lazy to perform post-mortem examinations, and that veterinarians are too prone in such cases to follow book teaching rather than their eyes. That the condition is very common is illustrated by the fact that canary breeders, poultrymen, and in one case a veterinarian, in their letters to me have described dozens, if not hundreds, of case histories that could apply to no other condition, still not one of them ever suspected that the affected birds might have been suffering from kidney disorders.

In all cases of chronic nephritis to come to my attention there has been a history of exposure or chilling associated with the appearance of the first symptoms. In the cases of some blackbirds, the bodies of which were sent to me for examination, there was also a history of metallic poisoning, resulting from the administration of medicine in metal drinkers. In many cases of chronic nephritis in canaries the condition develops following recovery from an attack of acute uremia. I have observed other cases in which the disease was chronic from the onset. The condition is more prevalent among females than males, and is sometimes associated with ovarian tumor.

The kidneys are usually enlarged two to three times normal size. They are smooth, glistening and bright yellow in color. Usually both kidneys are equally involved, though there are cases where only one kidney or a single lobe is affected. Such cases are only observed, however, where death is from other causes, since any bird with as much as one of its six kidney lobes in good condition will not die. The organs are bright yellow in color, swollen, glistening. The blood vessels stand out as bright red lines, but the ureters are invisible--in the normal kidney the ureters and their larger branches stand out as bold white lines. The urine contains epithelial ceils in various stages of degeneration, casts, fat globes, albuminous matter, urates in much smaller quantities than normal, uric acid crystals, and crystals of inorganic salts. Epithelial casts are sometimes found, but usually the material is so badly broken up that they are not easily identified. The urine of birds in the advanced stages of chronic nephritis gives a reaction for both sugar and albumen.* It is regrettable that the discharge from inflamed intestines also contains albumen and may, in some diseases (diphtheria for one), contain urates.

Symptoms: A bird in the early stages of nephritis appears to be but slightly out of condition. The appetite is good, but the digestion seems to be poor and the voided material usually contains a lot of fluid. The bird loses its taste for seed, but will eat large quantities of soft food and green food. If seed alone is given to these birds they will shell more of the seeds than they swallow--a common trait of birds suffering from digestive disturbances. The sick bird may sleep a little in the daytime, but this is not an usual symptom during the early stages of the illness. On warm days these birds appear as healthy and lively as any bird in your flock. They love to sit in the sun. As the disease progresses the bird sleeps in the daytime, acts constantly cold and loves to snuggle up against an electric light and sleep. I have found that by placing a 100-watt light in my cold flight, so arranged that the birds can cluster around it, the number of cases of uremia and nephritis are greatly reduced. All of the birds, sick and well alike, love to get right under the light and let it beat down on their backs, directly above the kidneys. The sick appear to be greatly benefited by this self-administered treatment. I have had some of them live for as long as two years. Sooner or later, however, a spell of cold weather gets them and they are found dead or dying.

As the illness progresses the symptoms of indigestion become more pronounced. The feces becomes dull-yellow in color and of more or less pasty consistency; the urine becomes thinner and more transparent than normal, of stringy, viscid consistency. It contains considerable albumen and is very irritating to the tissues of the vent and cloaca. The bird whips its tail after each passage. The feathers around the vent become fouled and have to be removed to keep them from blocking the opening. The female vent often protrudes to such an extent that she might be mistaken for a male. There is progressive emaciation; the bird becomes very weak, passes into a coma and dies.

Diagnosis: It is sometimes impossible to recognize all cases of nephritis during life. The symptoms of other chronic conditions, such as aspergillosis of the abdominal air sacs, streptococcus infection of the gall bladder and gall duct, tuberculosis, atrophy of the spleen, and at least a half-dozen distinct disorders of the digestive tract present symptoms closely resembling those of chronic nephritis. Where there is a history of chilling or exposure directly preceding the appearance of the first symptoms, or where the chronic symptoms followed an attack of acute uremia, the breeder is justified in assuming that the bird is suffering with nephritis and treating it accordingly.* I have found, however, that when a loopful of Gentian violet--a 0.5% solution to which two drops of normal sodium hydroxide solution has been added for each 100 cc--is permitted to run under the coverglass under which an emulsion of normal urine is being observed, crystalization of uric acid and phosphates takes place with the formation of crystals. It will be noticed that in the one case .the crystals have sharp angles and edges and in the other case all of the angles and edges are rounded. In normal urine there is little or no debris left after the crystalization; in abnormal urine there is considerable debris, it remains on the plan of the surface of the microscopic slide, however, while the crystals form on the under surface of the coverglass.

Treatment: It is possible that some birds recover from this condition. But since there is no .way of proving that the recovered birds were or were not suffering with nephritis, it is impossible to say that any particular line of treatment is of value. I have used diuretics and urotropine, potassium iodide, chinosol, cinchopen, and methylene blue. I have taken birds in a state of complete coma in acute uremia and brought them back to health and years of care-free existence; but, still, I cannot offer a line of treatment which may be depended upon to clear up this condition. The most effective of our kidney antiseptics is urotropine, but it is a very dangerous drug where birds are concerned, and its administration requires considerable care. Dissolve one 5-grain urotropine tablet in four ounces of water. Place the ailing bird in a cage by itself; arrange a glass plate under the perch upon which the bird sleeps, so as to catch the droppings for examination; then administer the urotropine solution in the drinking water, starting at a single drop to the ounce of drinking water and increasing the dose gradually, studying the effect upon the droppings each morning, searching carefully for the presence of blood. At the first appearance of blood or blood cells in the urine the dosage of urotropine solution should be reduced by one-third to one-half and continued at that figure for several months. This experimental treatment is necessary in every case because some birds suffering with nephritis drink enormous quantities of water while others drink very little, and an overdose of this drug will cause fatal hemorrhages from the kidneys. On bright sunny days the bird should be carried out into the sunshine for an hour or so; on chilly days he should be permitted to warm himself by an electric light. The diet should contain plenty of egg food, plenty of green food, and a good tonic-seed mixture. Under this careful treatment many suspected birds will recover. Some, of course, will die; and when their bodies are opened and the breeder sees those large yellow kidneys he is apt to feel that all of his efforts were just so much lost motion.

Acute uremia is a condition resulting from the complete suppression of the functions of the kidneys. The urinary products remain in the blood stream, where they exercise a poisonous reaction upon the body tissues, particularly nerve tissues. It is a rather common symptom of acute Bright's disease in man, and the condition I am about to describe might really be better named had I chosen to call it Acute Bright's disease of birds or Acute avian nephritis. I have avoided these names because the condition, at least at its inception, is not associated with inflammatory changes in the interstitial or medullary tissues of the kidneys. I have chosen the designation Uremia because it is my belief that in the beginning the condition is always purely functional and mechanical; that if injuries to the kidneys occur, they are always of a secondary nature; and that the entire phenomenon--depression, coma and death, is the result of uremic poisoning.

This condition is often confused with sporadic pneumonia by those who do not make a habit of performing post-mortem examinations. Many breeders, and others who should know better, having read that pneumonia is a highly fatal disease of birds, that the illness develops following exposure and is of short duration, jump to the conclusion that every bird to die under such circumstances is a victim of pneumonia. This attitude on the part of bird breeders and poultrymen can be overlooked; but what is hard to understand and overlook is the fact that not one of the books I have read on bird or poultry diseases, not one out of the hundreds of bulletins from state and governmental experimental stations, not one of the literally thousands of articles I have read in poultry and canary journals, has made any mention of this condition. It is hard to believe that the hundreds of trained investigators engaged in the study of poultry could have overlooked such a common condition. Since both poultrymen and aviculturists have written to me about many deaths which could have resulted from no other cause, I can hardly believe that anyone associated with birds in any way for any length of time could have failed to come in contact with it.

Cause: While the primary cause of the symptoms of uremia is the retention of waste products in the body, the real underlying cause is found in the conditions responsible for that retention. of these is the structure of the bird's kidneys, which is designed to handle urine in a thick, pasty state, which is possible only because of the bird's high body temperature. In every case of uremia to come to my attention, there has been a distinct history of chilling, of the bird sleeping in a draft or of a bird bathing in the open air during very cold weather, getting so wet that it could not fly to dry itself. We know that such conditions of exposure are responsible the greater part of nephritis in man. Why this is so, we do not know. In the case of birds, however, it is my opinion that lowering of the bird's body temperature caused the almost solid urine to crystallize in the small uriniferous tubes, thereby plugging them. It is my belief that a fall in body temperature causes the formation of these large crystals; that their points penetrate the wall of the small tubes; that the resulting congestion causes an increase in the pressure exerted by the surrounding tissue upon the tubes which results in the plugging becoming complete. Thus the functioning of the kidneys is suspended and uremic poisoning follows in short order.

Symptoms: There are two distinct forms of acute uremia. In the first form a bird that has been in perfect health is left in a draft, or, there may have been a sudden change in the weather which caused a draft of cold air to play upon the bird during the night while he was sleeping. A short time later he is discovered puffed up like a ball. He eats or drinks little, if at all. He shivers, seems cold and wants to sleep all the time. He will tuck his head back over his wing and go to sleep while you are talking to him. He becomes weaker by the minute, which is evident from the fact that when discovered the bird will usually be standing on one foot, is soon standing on both feet, and a little later has found it impossible to cling to the perch and has sought a corner of the cage where he finds it very difficult to keep from falling over. He does not sit on his heels and tail, however. He soon goes into a state of coma from which he can be only partially aroused. As the illness progresses toward a fatal termination, the breathing becomes more rapid and shallow, but at no time is there ever any gasping or open-mouthed breathing. There is no struggle of any kind. There are no droppings. The bird just sits quietly in his corner until he falls over, dead. Death may occur within from two to twenty-four hours of the onset of the attack. This form of the disease occurs almost exclusively in birds that are chilled during sleep.

In the second form of this condition, the bird may fly into a stream of cold air coming through a crack or a partly opened window; a bird may take a bath in the open air and get his feathers so wet he cannot fly to dry himself and thus stands in the cold air shivering until his owner notices him and takes him into the house. In either case the bird suffers from muscular cramps which appear to extend to the involuntary muscles of the kidneys. In any case, there is immediate and complete suspension of kidney functioning. I have seen canaries fly through a small shaft of cold air and fall to the floor as if they had been shot. Regardless of how the chilling occurs, the bird falls to the floor and lies there jerking. There may be a cataleptic contraction of the muscles of one side of the body which lasts for a few moments and is followed by a rhythmic jerking of all the muscles of the affected side. The beak opens, the eye blinks, the wing jerks down against the side, the foot jerks upward. The period of this jerking may be from ten to ninety per minute, but it is fairly uniform throughout the violent period of the illness. There is no kidney action, no droppings. Without treatment, the bird will die within from two to six hours. If kidney action can be re-established, the frequency of the jerking will become slower until it finally ceases, though this may take from two to forty-eight hours from the time the first droppings appear.

There may be a few punctiform hemorrhages in the brain and in some cases there is a slight effusion into the peritoneum and pericardium. The principal changes are in the kidneys, however. In the first form of the disease the kidneys have a gray granular appearance. There is not, as a rule, much, if any, enlargement. Under a ten diameter hand lens the grayness can be resolved into a series of alternating, white and purple, curved lines. The white lines are the plugged tubes; the purple lines are the highly congested medullary tissues. If the whole pelvis is fixed to the stage of a microscope and the kidney studied in situ in a thin, strong beam of light directed down upon it at an angle of about thirty degrees, it is possible to see the tubes and their contents. By using a 44x, high-working-distance objective and a 5 x eyepiece, it was possible to see the spear-shaped crystals with their points thrust through the walls of the tubes. By using a 10 x objective and a 15 x eyepiece, it was possible to get better light and wider view, though the image was not so good, and it could then be seen that above these points where the concretions of crystals plugged the tubes, the tubes were distended and varicosed--this was not noticed in cases where the bird died within two or three hours of the onset of the attack. In the spasmodic form of the disease, this plugging of the kidney tube was not observed.

Diagnosis: The symptoms of the spasmodic form of the disease cannot be mistaken. The only condition even remotely resembling it is cinchopin poisoning, which probably brings about a similar physiological condition. In any ease, the two conditions are amendable to the same lines of treatment. Too, the breeder knows whether or not he has been administering cinchopin. It is impossible to distinguish between the somnolent form of acute uremia and the early stages of sporadic pneumonia excepting by the droppings, and there are usually none in either case. The pneumonic bird does try to eat and drink a little at first and there may be a few droppings of a brown color. The uremic bird does not make any attempt to eat or drink, and if there are any droppings early in the attack, they will be of normal color. There are at least fifty cases of acute uremia in canaries for every case of sporadic pneumonia, so the safest course is to treat all such cases for uremia. This was true when written. I have now found that chest sounds give a reliable differentiation of these two conditions.

Treatment: If treated in time, all cases of acute uremia can be cured. The bird must be put in a warm place at once. I have found it a good plan to hang a 40-watt electric light inside the hospital cage and cover the cage with a cloth. Many birds will recover within a few hours without any other treatment. They should always be watched to see that they do not become over-heated, which would do more harm than good. Birds suffering from the somnolent form of the disease will usually snuggle up alongside of the light and go to sleep. If the light is hung so that they can get under it, they will lie down and spread their feathers and allow the light and heat to beat down upon their backs, over their kidneys. Sometimes this light treatment will start the kidneys functioning in a very short time, and birds apparently at the point of death may be eating and singing within an hour. These observations led me to arrange a box and a 100-watt light in my cold flight room, so that the birds could either snuggle against the light or crawl directly under it and sun themselves by it whenever they wished. There was an immediate and marked reduction in the number of uremic cases occurring in the room. Birds suffering from the spasmodic form of the disease are unable to get under the light or do anything else for themselves. They are Utterly helpless. I have found it advisable to wrap them in handkerchiefs and place them in a warm, but not too warm, place; since the handkerchief retains most of the body heat, less external heat is necessary.

When the symptoms of the uremic attack are spasmodic and the attack is discovered at once, the bird will always respond to the treatment just described, and the recovery, even though it takes thirty to forty hours to bring it about, will always be complete. There will be no aftereffects. There is no danger of the bird developing chronic nephritis following recovery. Most of the somnolent cases respond to this treatment, but in these cases the illness is not so apt to be discovered at its onset. Then, too, uncertainty of the diagnosis may cause delay in the application of the treatment, while all the time those big crystals are ripping the linings out of the kidney tubes. As a result, about fifty per cent of the birds affected with the somnolent form of acute uremia do not completely recover; they develop chronic nephritis as an aftereffect. Even some of these may regain a fair degree of good health for a while, but they are pretty certain to die of nephritis within two years.

Theory concerning the development of the uremic attack: I have noticed that cases of uremia developing during the breeding season are confined to males. From a single cage, hung facing a doorway, I lost two or three males every season for about four years. The cases always occurred during hot weather, and the attack always followed a sudden change in the weather occurring at night. Normally, no draft reached this cage for it was six feet from the door, but a sudden thunderstorm occurring at night would set up a circulation of air in the building of sufficient force to blow into this cage; and when that occurred I was pretty certain to find a very sick male in that cage next morning. Outside nest boxes were used, so that the hen, especially when she was standing over some well-grown chicks, was much more exposed to the draft than was the male sleeping in the back of the cage. None of these hens were affected. Their bodies received as much or more draft than the bodies of the males could have received, but their feet, down in the nest or among the babies, were protected.

Reasoning from this fact and from my studies of the uric acid crystals in the plugged tubes, I have come to believe that air blowing on a bird's feet during sleep caused a slow drop in body temperature, and that as the temperature falls the uric acid in the urine has a tendency to form larger and larger crystals, until a point is finally reached at which the concretions become so large that their points dig into the walls of the tubes. It must be remembered in this connection that the chilling which takes place during sleep, sudden as it may appear to be, is always more or less gradual. Its causes are of a nature which would be harmless to the waking bird--if they were violent enough to cause the bird to awaken, quit his perch and seek the floor of the cage, he would probably escape unharmed. We sometimes have storms of that nature in warmer climates and the birds come through them in good condition; it is the gentle, insidious draft playing on that unprotected foot which seems to be at the root of the whole trouble. And it is worth noting at this point, that while scientific investigators seem to have over-looked this condition entirely and practical breeders have been laboring under a misapprehension concerning its pathology, the latter have had sense enough to associate cause with effect and universally adopt the practice of covering the cages of their pet birds at night.

The phenomenon of the spasmodic form of acute uremia is something entirely different, so different, in fact, that the two conditions probably should have been discussed separately. Why a sudden and severe chill should cause violent muscular contractions and cramps seems to have escaped explanation--many swimmers who have experienced such attacks while in the water have not been lucky enough to escape with their lives, however, but it is such a condition we seem to be dealing with in spasmodic uremia. There are no changes in the kidney structure. It appears to me that cramping extends to the involuntary muscles of the kidneys and the uremic poisoning which follows, in some manner, tends to prevent these contracted muscles from relaxing. This conclusion is partly supported by several cases which were discovered at the moment of attack. The birds were taken in the hand and held with their backs up against a 100-watt lamp until they started to pant. I had these birds flying in less than an hour. But in other cases where a short but unavoidable delay had taken place between the onset of the attack and the application of heat, the application of strong heat to the back proved ineffective; they responded to the diurol treatment, however.

Info from the books "Diseases of Birds" by Robert Stroud and "Bird Diseases" by L. Arnell & I.F. Keymer.


E-Mail: berniehansen@sympatico.ca



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