Nonspecific disorder in which the kidney glomeruli are damaged, causing them to leak large amounts of protein.
Increasing oedema, albuminuria and raised blood pressure resulting from nephrosis.
Kidney damage characterized by increased permeability in renal tubules and loss of protein in the glomerular filtrate.
Degenerative renal lesions resulting from damage to the basement membrane of the glomeruli; commonly seen as a complication from systemic diseases such as diabetes mellitus, systemic lupus erythematosus, and multiple myeloma.
A combination of signs and symptoms caused by disorders that result in injury to the glomeruli (the filtering units of the kidneys). Damage to these structures results in abnormal excretion of protein in the urine.
A condition in which there is great loss of protein in the urine, reduced levels of albumin in the blood, and generalized swelling of the tissues due to edema. It can be caused by a variety of disorders, most usually glomerulonephritis.
The combination of proteinuria, hypoalbuminaemia (low blood level of albumin) and oedema. The primary cause is albumin leaking out of the blood into the urine through the glomerulus. When this exceeds the liver’s ability to make albumin, the plasma level falls and oedema results. The nephrotic syndrome is commonly the result of primary renal glomerular disease. It may also be a result of metabolic diseases such as diabetic glomerular sclerosis and amyloidosis, or of systemic autoimmune diseases such as systemic lupus erythematosus (SLE) and polyarteritis nodosa. It may complicate malignant diseases such as myelomatosis and Hodgkin’s disease. It is sometimes caused by nephrotoxins such as gold or mercury and certain drugs, and it may be the result of certain infections such as malaria and crohn’s disease. Treatment depends on the cause. In glomerulonephritis, particularly a problem for children, courses of corticosteroids and other anti-inflammatory agents may be needed.
A condition marked by increased renal glomerular permeability to proteins, resulting in massive loss of proteins in the urine, edema, hypoalbuminemia, hyperlipidemia, and hypercoagulability. Several different types of glomerular injury can cause the syndrome, including membranous glomerulopathy, minimal change disease (lipoid nephrosis), focal segmental glomerulosclerosis, glomerulonephritis, and membranoproliferative glomerulonephritis. These pathological findings in the kidney result from a broad array of diseases such as diabetic injury to the glomerulus, amyloidosis, immune-complex deposition disease, vasculitis, systemic lupus erythematosus, allergic reactions, infections, and toxic injury to the kidneys by drugs or heavy metals. The disease’s prognosis depends on the cause. For example, if the cause is exposure to a drug or toxin, the removal of that substance may be curative. When the disease results from glomerulosclerosis caused by AIDS, death may occur within months. Renal biopsy usually is needed to determine the precise histological cause, treatment, and prognosis. Idiopathic NS is diagnosed when the known causes of NS have been excluded. It is usually diagnosed in adults by use of renal biopsy. Causes are classified according to the changes found in the capillaries of the glomerulus when examined by use of electron microscopy.
A cluster of symptoms arising due to impairment of the kidney’s filtering units, known as glomeruli, leading to significant protein loss from the blood into the urine.
A set of symptoms and indications arise due to glomerular damage (the filtering components of the kidney). This damage leads to pronounced proteinuria (the passage of protein from the blood into the urine), diminished levels of protein in the blood, and edema.
Nephrotic syndrome can develop due to diabetes mellitus, amyloidosis (accumulation of abnormal protein known as amyloid in tissues), or various forms of glomerulonephritis (inflammation of the glomeruli). It can also be a result of intense hypertension (high blood pressure), toxic reactions (such as exposure to mercury or cadmium), or adverse responses to medications, including gold or penicillamine.
Nephrotic syndrome can also arise as a complication of infections occurring elsewhere in the body, like hepatitis B or malaria. Among children, the syndrome is frequently linked to a condition called minimal change glomerulonephritis.
The indications of nephrotic syndrome emerge gradually over a span of days or weeks and intensify as the urinary protein loss increases. Initial signs encompass frothy urine and reduced urine output. The primary symptom entails swelling in the legs and face due to edema (fluid buildup in the tissues). Fluid might also accumulate in the chest cavity, resulting in pleural effusion and breathlessness, or in the abdomen, leading to ascites. Fatigue and diminished appetite (culminating in weight loss) may also manifest.
Diagnosis necessitates blood tests, along with microscopic analysis of the urine to assess the quantity and nature of protein loss within a 24-hour span. In the majority of instances, performing a kidney biopsy (extracting a small tissue sample for microscopic scrutiny) is also essential to pinpoint the precise cause and guide treatment choices.
Treatment is focused on addressing the root cause of the condition. A low-sodium diet might be advised, and diuretic medications could be administered to alleviate edema. Intravenous protein supplementation might be necessary, although its effects are temporary. Corticosteroid medications may also be prescribed, often proving effective in managing nephrotic syndrome during childhood.
The prognosis for an individual with nephrotic syndrome hinges on the degree of kidney damage. Repeated episodes might arise even after treatment. Complications related to excessive blood clotting are frequent and may necessitate anticoagulant therapy. Infections can be a consequence of immunoglobulin loss into the urine. Nephrotic syndrome is typically linked to elevated cholesterol levels, heightening the risk of myocardial infarction (heart attack) due to atherosclerosis (accumulation of fatty deposits in artery walls). In severe cases, chronic kidney failure may emerge, eventually leading to irreversible loss of kidney function.