Because of the importance of osmotic forces in determining fluid distribution within the body, an important attribute of body fluid is its overall osmotic concentration, or osmolality. This depends on the concentration of solutes. While all solutes contribute to osmolality, small particles such as sodium or chloride ions are influential out of all proportion to their weight, and indeed account for over 90 percent of the osmolality of plasma. In the context of renal disease, changes in osmolality depend largely on how the kidney handles water. When the kidney either is incapable of conserving water or is not stimulated by ADH of the pituitary to do so, water is lost from the body, and a state of water depletion develops, characterized by increasing osmolality of body fluid. At other times, the kidneys may retain too much water, especially when too much hormone is present; in this case, water excess results, giving a clinical state of water intoxication, with decreased osmolality of body fluids.

Another important general property of body fluid is its degree of acidity or alkalinity. The kidneys are involved in the excretion of hydrogen ions, and imperfect function leads to their retention, the state of so-called renal acidosis. Renal acidosis may occur as part of general renal failure or as a specific disease of the renal tubules, one of whose functions is to convert the slightly alkaline glomerular filtrate into the (usually) acidic urine.

Apart from these general changes in body fluid, the pattern of individual constituents can be distorted in renal disease. For many substances, the problem is one of failure of excretion, with consequent increased concentration in body fluids. Insofar as excretion is achieved by filtration, the rise in concentration may assist excretion, permitting prolonged states of balance, at the cost of increased, but often tolerable, levels of concentration. For example, an individual in renal failure must put out as much urea as a healthy individual taking the same diet; but that person can only do so at a blood-urea concentration of 100 milligrams per 100 millilitres, instead of a normal blood-urea of 25 milligrams per 100 millilitres. Substances whose concentration increases in this way include urea, creatinine, uric acid, phosphate, sulfate, urochrome, and indeed all the usual constituents of urine apart from those that are “regulated” rather than simply “excreted.” Potassium should be mentioned because of the special danger associated with its retention, which can lead to fatal irregularity of cardiac action. This is a recognized danger of acute renal failure, now commonly prevented by use of the artificial kidney and its semipermeable membranes, and sometimes by the use of resins that will take up potassium in the alimentary tract.

Normal urine contains traces of protein, and in many forms of renal disease there is an increased excretion of protein in the urine, usually representing an increased permeability of the tuft of capillaries forming the glomerulus. This increased proteinuria (often, but less correctly, known as albuminuria) generally amounts to 0.5 gram per day or more. When it exceeds five grams per day and persists at this level, the loss of protein in the urine exceeds the capacity of the liver to produce new protein from the available materials; the concentration of protein in the blood decreases, and this leads to an increasing outflow of fluid from the bloodstream into the tissues (there is normally an equilibrium between the physical pressure in the capillaries, which tends to force fluids out, and the osmotic pressure of plasma proteins, the effect of which is to hold fluid in). This balance of forces is upset by a deficit of plasma proteins. The general loss of fluid into the tissues leads to massive edema, to which the kidneys contribute further by retaining salt and water. The combination of high levels of protein in the urine, low protein levels in the blood, and consequent edema is known as the nephrotic syndrome. This is a good example of a syndrome, defined as a recognizable pattern of manifestations that has not one but a number of possible causes. Other examples of syndromes in renal disease are acute renal failure and chronic renal failure.

Disorders of urine flow

If little or no urine appears, it may be because the kidneys are forming little urine (oliguria) or none (anuria); or it may represent a holdup in the bladder or urethra affecting the outflow from both kidneys. About one person in 500 is born with only one kidney, and loss of a kidney from disease or accident is not rare. The loss of a single kidney does not substantially affect an individual’s ability to eliminate wastes, as long as the other kidney functions normally. In cases in which complete obstruction of the remaining ureter occurs, patients will experience effects similar to obstruction of the entire lower urinary tract. Partial or complete failure to form urine is treated in the section on acute renal failure, obstructive conditions in the section on diseases of the urinary tract.

In instances of damage to nervous control, certain typical clinical situations may be differentiated, corresponding to different modes of disordered urinary flow: (1) Lack of conscious inhibition of micturition because of damage to the cerebral cortex or, more commonly, from psychological causes results in a need to micturate that cannot be suppressed even though the bladder volume may be quite small; micturition is precipitate and continues until the bladder is empty. (2) Transverse lesions or other damage to the spinal cord above the sacral reflex centres that cause paralysis of the lower half of the body produce at first a bladder that is atonic (lacking in physiological tone). This bladder becomes greatly distended; the detrusor relaxes and reflex micturition is abolished. Pressure finally rises sufficiently to overcome the spasm of the sphincters and urine is voided in small amounts. Further accumulation and partial voiding of the overflow recur (overflow incontinence). Under these conditions the bladder readily becomes inflamed, which may cause disability or death from chronic ascending urinary infection. Intermittent drainage of the bladder with a catheter may be necessary, or firm pressure on the lower abdominal wall may be used to avoid overdistension and to develop an “automatic” bladder after some time. This is a small capacity organ (around 150 millilitres) with frequent emptying; there is reflex control mediated through the sacral segments of the spinal cord; the higher centres do not restrain the detrusor, and the internal sphincter relaxes more readily. Voluntary assistance from the abdominal muscles helps in this situation if these too have not been paralyzed. There is, however, always some residual urine from incomplete emptying and a risk of infection. In some cases, pressure building within the bladder can be transmitted to the kidneys; without medications or more frequent bladder emptying to relieve the pressure, the kidneys will incur damage. (3) In contrast, there is the isolated, or “autonomous,” bladder resulting from damage to the central nervous system below the sacral cord reflex centres or to the nerves supplying the bladder and urethra. The bladder becomes tense but contracts only weakly so that, while small amounts of urine are voided, the residual urine may be as high as 200–300 millilitres. This condition is known as active incontinence as opposed to the overflow incontinence of the automatic bladder. Here again, more effective emptying of the bladder by catheter drainage may be helpful.

Pain associated with urination (dysuria) can arise from bladder distension, which is then relieved by effective micturition; from inflammation of the lower urinary tract, commonly due to infection but rarely caused by chemical irritants in the urine; and from mechanical irritation by tumour or during the passage of stones. Dysuria is commonly, but not necessarily, associated with frequency of urination. This in turn may represent either an irritable or contracted bladder; or the actual amount of urine formed may be unusually large (polyuria), in which case voiding is likely to be painless. Sometimes polyuria may not be noticed by day but may manifest itself in the need to micturate on several occasions during the night (nocturia). The acute onset of dysuria and frequency suggests urinary infection; sustained polyuria is more likely to be due to renal failure (defective concentrating power) or to diabetes. In those who drink beverages into the night, nocturia is physiological.

Incontinence, the involuntary passage of urine (or feces), may be due to a faulty nerve supply, which either leaves the sphincters relaxed or allows them to be overcome by distension of the bladder. Comatose and disturbed patients, especially among the elderly, are commonly incontinent. Apart from nerve lesions, the sphincters that normally prevent the escape of urine may be damaged by repeated childbirth, by the growth of the prostate, or by other distortions of the bladder neck. Medications to relax the bladder and increase its capacity may be helpful. Alternately, more complete bladder emptying by intermittent catheterization may limit the amount of urine leakage. Procedures have been devised to stimulate the sphincters electrically, when their nerve supply is damaged; or to stimulate the bladder to empty itself at set times. For chronic incontinence, however, devices to catch the urine and prevent soiling of clothing are the most practical.