see cast nephropathy.
The cortex contains specialized capillaries called glomeruli, which, together with a series of tubules, make up the nephrons, the filtering units of the kidney. The nephrons filter blood under pressure and then selectively reabsorb water and certain other substances back into the blood. Urine is formed from substances that are not reabsorbed. The urine is conducted through tubules to the renal pelvis (the central collecting area of the kidney) and then through tubes called ureters to the bladder.
The kidneys also regulate the body’s fluid balance.
To do this, the kidneys excrete excess water, and when water is lost from the body (for example as a result of sweating), they conserve it (see ADH).
In addition, the kidneys control the body’s acid–base balance by adjusting urine acidity.
The kidneys are also involved in hormonal regulation of red blood cell production and blood pressure.... kidney
K
Diagram of glomerulus (Malpighian corpuscle).
Fortunately the body has two kidneys and, as most people can survive on one, there is a good ‘functional reserve’ of kidney tissue.
Symptoms Many patients with kidney disorders do not have any symptoms, even when the condition is quite advanced. However,
others experience loin pain associated with obstruction (renal colic) or due to infection; fevers; swelling (oedema), usually of the legs but occasionally including the face and arms; blood in the urine (haematuria); and excess quantities of urine (polyuria), including at night (nocturia), due to failure of normal mechanisms in the kidney for concentrating urine. Patients with chronic renal failure often have very di?use symptoms including nausea and vomiting, tiredness due to ANAEMIA, shortness of breath, skin irritation, pins and needles (paraesthesia) due to damage of the peripheral nerves (peripheral neuropathy), and eventually (rarely seen nowadays) clouding of consciousness and death.
Signs of kidney disease include loin tenderness, enlarged kidneys, signs of ?uid retention, high blood pressure and, in patients with end-stage renal failure, pallor, pigmentation and a variety of neurological signs including absent re?exes, reduced sensation, and a coarse ?apping tremor (asterixis) due to severe disturbance of the body’s normal metabolism.
Renal failure Serious kidney disease may lead to impairment or failure of the kidney’s ability to ?lter waste products from the blood and excrete them in the urine – a process that controls the body’s water and salt balance and helps to maintain a stable blood pressure. Failure of this process causes URAEMIA – an increase in urea and other metabolic waste products – as well as other metabolic upsets in the blood and tissues, all of which produce varying symptoms. Failure can be sudden or develop more slowly (chronic). In the former, function usually returns to normal once the underlying cause has been treated. Chronic failure, however, usually irreparably reduces or stops normal function.
Acute failure commonly results from physiological shock following a bad injury or major illness. Serious bleeding or burns can reduce blood volume and pressure to the point where blood-supply to the kidney is greatly reduced. Acute myocardial infarction (see HEART, DISEASES OF) or pancreatitis (see PANCREAS, DISORDERS OF) may produce a similar result. A mismatched blood transfusion can produce acute failure. Obstruction to the urine-?ow by a stone (calculus) in the urinary tract, a bladder tumour or an enlarged prostate can also cause acute renal failure, as can glomerulonephritis (see below) and the haemolytic-uraemia syndrome.
HYPERTENSION, DIABETES MELLITUS, polycystic kidney disease (see below) or AMYLOIDOSIS are among conditions that cause chronic renal failure. Others include stone, tumour, prostatic enlargement and overuse of analgesic drugs. Chronic failure may eventually lead to end-stage renal failure, a life-threatening situation that will need DIALYSIS or a renal transplant (see TRANSPLANTATION).
Familial renal disorders include autosomal dominant inherited polycystic kidney disease and sex-linked familial nephropathy. Polycystic kidney disease is an important cause of renal failure in the UK. Patients, usually aged 30–50, present with HAEMATURIA, loin or abdominal discomfort or, rarely, urinary-tract infection, hypertension and enlarged kidneys. Diagnosis is based on ultrasound examination of the abdomen. Complications include renal failure, hepatic cysts and, rarely, SUBARACHNOID HAEMORRHAGE. No speci?c treatment is available. Familial nephropathy occurs more often in boys than in girls and commonly presents as Alport’s syndrome (familial nephritis with nerve DEAFNESS) with PROTEINURIA, haematuria, progressing to renal failure and deafness. The cause of the disease lies in an absence of a speci?c ANTIGEN in a part of the glomerulus. The treatment is conservative, with most patients eventually requiring dialysis or transplantation.
Acute glomerulonephritis is an immune-complex disorder due to entrapment within glomerular capillaries of ANTIGEN (usually derived from B haemolytic streptococci – see STREPTOCOCCUS) antibody complexes initiating an acute in?ammatory response (see IMMUNITY). The disease affects children and young adults, and classically presents with a sore throat followed two weeks later by a fall in urine output (oliguria), haematuria, hypertension and mildly abnormal renal function. The disease is self-limiting with 90 per cent of patients spontaneously recovering. Treatment consists of control of blood pressure, reduced ?uid and salt intake, and occasional DIURETICS and ANTIBIOTICS.
Chronic glomerulonephritis is also due to immunological renal problems and is also classi?ed by taking a renal biopsy. It may be subdivided into various histological varieties as determined by renal biospy. Proteinuria of various degrees is present in all these conditions but the clinical presentations vary, as do their treatments. Some resolve spontaneously; others are treated with steroids or even the cytotoxic drug CYCLOPHOSPHAMIDE or the immunosuppressant cyclosporin. Prognoses are generally satisfactory but some patients may require renal dialysis or kidney transplantation – an operation with a good success rate.
Hydronephrosis A chronic disease in which the kidney becomes greatly distended with ?uid. It is caused by obstruction to the ?ow of urine at the pelvi-ureteric junction (see KIDNEYS – Structure). If the ureter is obstructed, the ureter proximal to the obstruction will dilate and pressure will be transmitted back to the kidney to cause hydronephrosis. Obstruction may occur at the bladder neck or in the urethra itself. Enlargement of the prostate is a common cause of bladder-neck obstruction; this would give rise to hypertrophy of the bladder muscle and both dilatation of the ureter and hydronephrosis. If the obstruction is not relieved, progressive destruction of renal tissue will occur. As a result of the stagnation of the urine, infection is probable and CYSTITIS and PYELONEPHRITIS may occur.
Impaired blood supply may be the outcome of diabetes mellitus and physiological shock, which lowers the blood pressure, also affecting the blood supply. The result can be acute tubular necrosis. POLYARTERITIS NODOSA and SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) may damage the large blood vessels in the kidney. Treatment is of the underlying condition.
Infection of the kidney is called pyelonephritis, a key predisposing factor being obstruction of urine ?ow through the urinary tract. This causes stagnation and provides a fertile ground for bacterial growth. Acute pyelonephritis is more common in women, especially during pregnancy when bladder infection (CYSTITIS) spreads up the ureters to the kidney. Symptoms are fever, malaise and backache. Antibiotics and high ?uid intake are the most e?ective treatment. Chronic pyelonephritis may start in childhood as a result of congenital deformities that permit urine to ?ow up from the bladder to the kidney (re?ux). Persistent re?ux leads to recurrent infections causing permanent damage to the kidney. Specialist investigations are usually required as possible complications include hypertension and kidney failure.
Tumours of the kidney are fortunately rare. Non-malignant ones commonly do not cause symptoms, and even malignant tumours (renal cell carcinoma) may be asymptomatic for many years. As soon as symptoms appear – haematuria, back pain, nausea, malaise, sometimes secondary growths in the lungs, bones or liver, and weight loss – urgent treatment including surgery, radiotherapy and chemotherapy is necessary. This cancer occurs mostly in adults over 40 and has a hereditary element. The prognosis is not good unless diagnosed early. In young children a rare cancer called nephroblastoma (Wilm’s tumour) can occur; treatment is with surgery, radiotherapy and chemotherapy. It may grow to a substantial size before being diagnosed.
Cystinuria is an inherited metabolic defect in the renal tubular reabsorption of cystine, ornithine, lysine and arginine. Cystine precipitates in an alkaline urine to form cystine stones. Triple phosphate stones are associated with infection and may develop into a very large branching calculi (staghorn calculi). Stones present as renal or ureteric pain, or as an infection. Treatment has undergone considerable change with the introduction of MINIMALLY INVASIVE SURGERY (MIS) and the destruction of stone by sound waves (LITHOTRIPSY).... kidneys, diseases of
Adult kidneys have a smooth exterior, enveloped by a tough ?brous coat that is bound to the kidney only by loose ?brous tissue and by a few blood vessels that pass between it and the kidney. The outer margin of the kidney is convex; the inner is concave with a deep depression, known as the hilum, where the vessels enter. The URETER, which conveys URINE to the URINARY BLADDER, is also joined at this point. The ureter is spread out into an expanded, funnel-like end, known as the pelvis, which further divides up into little funnels known as the calyces. A vertical section through a kidney (see diagram) shows two distinct layers: an outer one, about 4 mm thick, known as the cortex; and an inner one, the medulla, lying closer to the hilum. The medulla consists of around a dozen pyramids arranged side by side, with their base on the cortex and their apex projecting into the calyces of the ureter. The apex of each pyramid is studded with tiny holes, which are the openings of the microscopic uriniferous tubes.
In e?ect, each pyramid, taken together with the portion of cortex lying along its base, is an independent mini-kidney. About 20 small tubes are on the surface of each pyramid; these, if traced up into its substance, repeatedly subdivide so as to form bundles of convoluted tubules, known as medullary rays, passing up towards the cortex. One of these may be traced further back, ending, after a tortuous course, in a small rounded body: the Malpighian corpuscle or glomerulus (see diagram). Each glomerulus and its convoluted tubule is known as a nephron, which constitutes the functional unit of the kidney. Each kidney contains around a million nephrons.
After entering the kidney, the renal artery divides into branches, forming arches where the cortex and medulla join. Small vessels come o? these arches and run up through the cortex, giving o? small branches in each direction. These end in a tuft of capillaries, enclosed in Bowman’s capsule, which forms the end of the uriniferous tubules just described; capillaries with capsule constitute a glomerulus.
After circulating in the glomerulus, the blood leaves by a small vein, which again divides into capillaries on the walls of the uriniferous tubules. From these it is ?nally collected into the renal veins and then leaves the kidney. This double circulation (?rst through the glomerulus and then around the tubule) allows a large volume of ?uid to be removed from the blood in the glomerulus, the concentrated blood passing on to the uriniferous tubule for removal of parts of its solid contents. Other arteries come straight from the arches and supply the medulla direct; the blood from these passes through another set of capillaries and ?nally into the renal veins. This circulation is con?ned purely to the kidney, although small connections by both arteries and veins exist which pass through the capsule and, joining the lumbar vessels, communicate directly with the aorta.
Function The kidneys work to separate ?uid and certain solids from the blood. The glomeruli ?lter from the blood the non-protein portion of the plasma – around 150–200 litres in 24 hours, 99 per cent of which is reabsorbed on passing through the convoluted tubules.
Three main groups of substances are classi?ed according to their extent of uptake by the tubules:
(1) SUBSTANCES ACTIVELY REABSORBED These include amino acids, glucose, sodium, potassium, calcium, magnesium and chlorine (for more information, see under separate entries).
(2) SUBSTANCES DIFFUSING THROUGH THE TUBULAR EPITHELIUM when their concentration in the ?ltrate exceeds that in the PLASMA, such as UREA, URIC ACID and phosphates.
(3) SUBSTANCES NOT RETURNED TO THE BLOOD from the tubular ?uid, such as CREATINE, accumulate in kidney failure, resulting in general ‘poisoning’ known as URAEMIA.... structure each kidney is about 10 cm long,
Kidney biopsy is performed to investigate and diagnose serious kidney disorders, such as glomerulonephritis, proteinuria, nephrotic syndrome, and acute kidney failure, or to assess the kidneys’ response to treatment.
There are 2 basic techniques: percutaneous needle biopsy, in which a hollow needle is passed through the skin into the kidney under local anaesthesia; and open surgery under general anaesthesia.... kidney biopsy
Formula. Corn Silk 3; Plantain (Plantago major L) 2; Golden Rod 1; Hydrangea 1; Valerian half. Dosage: thrice daily before meals. Liquid Extracts: 1 teaspoon. Tinctures: 2 teaspoons. Powders: two 00 capsules or one-third teaspoon. This may be used as a basic combination to be adapted to a changing clinical picture.
Treatment by a general medical practitioner or oncologist. ... cancer – kidney
Urinalysis is a simple test in which a urine sample is examined under a microscope for blood cells, pus cells, and casts (cells and mucous material that accumulate in the tubules of the kidneys and pass into the urine).
Urine may be tested for substances, such as proteins, that leak into the urine when the kidneys are damaged.
Kidney function can be assessed by measuring the concentration in the blood of substances, such as urea and creatinine, that the kidneys normally excrete.
Kidney function may also be assessed by kidney imaging techniques.... kidney function tests
Polycystic kidney disease is distinguished from multiple simple kidney cysts, which occur commonly with age.
There are 2 types of polycystic disease.
The most common usually becomes apparent in middle age, producing abdominal swelling, pain, and blood in the urine.
As the disease progresses, hypertension and kidney failure may result.
The rare type causes enlargement of the kidneys and kidney failure in infants and young children.
There is no effective treatment for preserving kidney function in either type, but symptoms of kidney failure can be treated by dialysis and kidney transplant.... kidney, polycystic
Plasma cells are a type of B-lymphocyte that produce immunoglobulins, which help protect against infection. In multiple myeloma, the proliferating plasma cells produce excessive amounts of one type of immunoglobulin, while production of other types is impaired. This makes infection more likely.Proliferation of the abnormal cells causes pain and destroys bone tissue.
Affected vertebrae may collapse and compress nerves, causing numbness or paralysis. Blood calcium levels increase as bone is destroyed, as may the level of one or more immunoglobulins. These changes in the blood may damage the kidneys, leading to kidney failure. There may also be anaemia and a tendency for abnormal bleeding.
The disease is diagnosed by a bone marrow biopsy, by blood tests or urinalysis, and by X-rays. Treatment includes the use of anticancer drugs, radiotherapy, and supportive measures, including blood transfusions, antibiotic drugs, and analgesic drugs.... multiple myeloma
Autosomal dominant polycystic kidney disease (ADPKD) affects between 1 in 400 and 1 in 1000 individuals and is one of the most common hereditary diseases. Two types have been defined. ADPKD 1 is the commonest and responsible for about 85% of cases. It is due to a mutation in the PKD1 gene on chromosome 16, which encodes polycystin 1, an *ion-channel-regulating protein. ADPKD2 is due to a mutation in the PKD2 gene on chromosome 4, which encodes the protein polycystin 2, a calcium-release channel. ADPKD2 tends to be a milder disease with later presentation.
ADPKD is a multisystem disorder that is also associated with cyst formation in other organs (particularly the liver), cardiovascular disorders, and colonic diverticular disease. Renal disease presents in early adult life with haematuria, loin pain, urinary tract infection, hypertension, renal stone disease, or the finding of a mass in the abdomen. Other cases are identified by family contact tracing; the findings of a few cysts on renal ultrasonography in a young adult with a family history of ADPKD is highly suggestive of the disease. Renal disease is progressive and about 50% of patients will have reached end-stage by the time they enter their seventh decade. The progress of the renal failure can be slowed by good blood pressure control. In the UK, patients with ADPKD are responsible for 5–10% of the total on renal replacement therapy.
There are a number of separate rare autosomal dominant conditions other than ADPKD1 and ADPKD 2 that can present with polycystic kidneys. These include *von Hippel-Lindau disease and *tuberous sclerosis.... polycystic disease of the kidneys
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