Proteinuria, also known as urine protein, is a common clinical abnormality in the urine, detected by a routine urinalysis. A 24-hour urine protein level exceeding 150 mg is considered proteinuria. If the urinalysis is negative, but specific, more sensitive methods detect excessive albumin in the urine (>30 mg/24 hours), this is considered microalbuminuria. If the urine protein level exceeds 3.5 g/24 hours, this is considered macroalbuminuria. Excessive proteinuria can cause foamy urine. Proteinuria is seen in various primary and secondary kidney diseases, as well as urinary tract infections, tuberculosis, stones, tumors, and even in conditions such as exercise and fever (in the absence of urinary tract disease). With increased health awareness in recent years, routine physical examinations have become widespread, and many cases of chronic kidney disease (CKD) are discovered, diagnosed, and treated promptly through the detection of proteinuria in urine tests.
Epidemiology
ContagiousNot contagious.
symptom
Typical manifestations
1. Common symptoms
In the early stages, proteinuria presents with no obvious symptoms and is often only detected through examination. As protein levels continue to rise, foamy urine may develop during urination, with persistent foam. If combined with certain kidney diseases, symptoms may include lower back pain, lower limb edema, and facial edema.
2. Type of proteinuria
(1) Physiological proteinuria
① Functional proteinuria: transient proteinuria caused by stressful conditions such as strenuous exercise, fever, and tension, more common in adolescents. Qualitative test urine protein usually does not exceed (+).
② Orthostatic proteinuria: common in adolescents during puberty. Proteinuria occurs in upright and lordotic postures and disappears in supine position. The general protein excretion is <1g/d.
(2) Glomerular proteinuria
Proteinuria is caused by damage to the glomerular filtration membrane, increased permeability, and the filtration of plasma proteins that exceeds the renal tubular reabsorption capacity. Clinically, proteinuria is the most common form of proteinuria and is often seen in primary or secondary glomerular diseases, such as acute nephritis, rapidly progressive nephritis, chronic nephritis, IgA nephropathy, nephrotic syndrome, lupus nephritis, purpuric nephritis, diabetic nephropathy, hypertensive nephropathy, tumor-induced nephropathy, renal amyloidosis, toxic nephropathy, and renal damage caused by infection. It can also be seen in congenital nephritis, renal circulatory disorders, renal hypoxia, and accelerated renal blood flow.
(3) Tubular proteinuria
When the renal tubular structure or function is damaged, the renal tubules are unable to reabsorb normally filtered small molecular weight proteins, resulting in protein excretion in the urine. This is called tubular proteinuria. This condition is commonly seen in tubular-interstitial lesions caused by various factors, such as pyelonephritis, interstitial nephritis, reflux nephropathy, uric acid nephropathy, renal tubular acidosis, heavy metal poisoning, Fanconi syndrome, hypokalemic nephropathy, renal medullary cystic changes, radiation nephritis, analgesic nephropathy, and post-renal transplant rejection.
(4) Overflow proteinuria
Proteinuria is caused by an abnormal increase in small molecular weight blood proteins, such as multiple myeloma light chain proteins, hemoglobin, and myoglobin, which are filtered out of the glomeruli and exceed the renal tubular reabsorption threshold. All of these proteins can be completely reabsorbed by the renal tubules. Bence Jones protein is commonly seen in multiple myeloma, but is also seen in macroglobulinemia, heavy and light chain diseases, amyloidosis, and occasionally in monocytic leukemia. Hemoglobin or myoglobin may be seen in cases of extensive muscle tissue damage and excessive hemolysis. Elevated FDP in the urine also constitutes overflow proteinuria in cases of renal transplant rejection and disseminated intravascular coagulation.
(5) Secretory proteinuria
Proteinuria is caused by the leakage of proteins secreted by the renal tubules and lower urinary tract or other proteins into the urine. It is associated with immune reactions and urinary tract infections.
(6) Tissue proteinuria
These primarily refer to soluble tissue decomposition metabolites secreted by the kidneys, as well as structural proteins released during necrosis of the kidneys and urinary tract in conditions such as poisoning, ischemia, inflammation, or tumors. For example, in glomerulonephritis, glomerular basement membrane antigens, renal tubular brush border antigens, and various enzymes are excreted in the urine; in tumors, specific tumor-related antigens can be detected in the urine.
(7) Mixed proteinuria
Clinically, the coexistence of two types of proteinuria (e.g., glomerular proteinuria and tubular proteinuria) is called mixed proteinuria. Glomerulonephritis can affect both the glomeruli and tubules, resulting in both glomerular and tubular proteinuria. Mixed proteinuria is also common in chronic renal failure.
reason
Overview
Proteinuria is primarily caused by abnormal renal filtration function due to various primary and secondary kidney diseases. It can also be seen in certain systemic diseases and physiological conditions such as strenuous exercise and fever.
Cause of symptoms
1. Kidney disease
(1) Primary renal disease
Such as acute nephritis, pyelonephritis, interstitial nephritis, glomerulosclerosis, IgA nephropathy, nephrotic syndrome, etc.
(2) Secondary kidney disease
It is common in secondary kidney diseases such as systemic lupus erythematosus, Henoch-Schonlein purpura, diabetes, infective endocarditis, hypertension, acute rheumatic fever, primary Sjögren’s syndrome, systemic sclerosis, polymyositis, dermatomyositis, leukemia, lymphoma, and hyperuricemia.
2. Systemic diseases
Such as hemolytic anemia, crush syndrome, multiple myeloma, plasma cell disease, light chain disease, primary monoclonal gammopathy, macroglobulinemia, etc.
3. Physiological factors
Vigorous exercise (or fatigue), cold, fever, mental stress, sympathetic nerve excitement, etc. can cause temporary proteinuria; in addition, proteinuria may also occur due to increased local venous pressure caused by the protruding spine compressing the left renal vein when the human body is in an upright position.
4. Others
Heavy metal poisoning, pesticide poisoning, chemical organic solvent poisoning; drug-induced kidney damage, such as antibiotics, non-steroidal anti-inflammatory drugs, etc.; after kidney transplantation, etc., can also lead to the occurrence of proteinuria.
Common diseases
Acute nephritis, pyelonephritis, interstitial nephritis, glomerulosclerosis, IgA nephropathy, nephrotic syndrome, systemic lupus erythematosus, Henoch-Schonlein purpura, diabetes mellitus, infective endocarditis, hypertension, acute rheumatic fever, primary Sjögren’s syndrome, systemic sclerosis, polymyositis, dermatomyositis, leukemia, lymphoma, hyperuricemia, hemolytic anemia, crush syndrome, multiple myeloma, plasma cell disease, light chain disease, primary monoclonal gammopathy, macroglobulinemia, etc.
Seeking medical treatment
Outpatient indications
If proteinuria is detected during examination, or if the following conditions occur, you should consult a doctor promptly:
1. Continuous or recurring urinary discomfort such as frequent urination, urgency, pain, and incomplete urination;
2. Accompanied by turbid urine, gross hematuria, oliguria or anuria;
3. Abnormal urethral discharge;
4. Accompanied by systemic symptoms such as fever, fatigue, edema, low back pain, rash, and weight loss;
5. Have a history of long-term exposure to heavy metals, pesticides and other toxic substances;
6. Examination revealed other urine abnormalities such as casts;
7. Other severe, persistent or progressive symptoms and signs occur.
Treatment departmentPatients can go to the nephrology department or urology department for treatment in time.
Medical preparation
1. Make an appointment in advance and bring your ID card, medical insurance card, medical card, etc.
2. You may need to undergo kidney function tests. Please be sure to fast after 10 pm the night before the test and have your blood drawn on an empty stomach the next morning.
3. A routine urine test may also be required. Avoid strenuous exercise and sexual intercourse before the test, and women should avoid it during menstruation to prevent it from affecting the test results.
4. If you have had medical treatment recently, please bring relevant medical records, examination reports, laboratory test results, etc.
5. If you have taken some medicine to relieve symptoms recently, you can bring the medicine box with you.
6. Family members can be arranged to accompany the patient to seek medical treatment.
7. Patients can prepare a list of questions they want to ask in advance.
What questions might a doctor ask a patient?
1. When did you first notice your proteinuria symptoms? Have your symptoms changed over time?
2. In addition to proteinuria, do you also have other discomforts such as frequent urination, urgency, fever, etc.?
3. Have you ever had proteinuria? What caused it?
4. Have you ever used medication for treatment? What medication? How effective was it?
5. Have you ever suffered from or are you currently suffering from kidney diseases such as glomerulonephritis or pyelonephritis?
6. Do you have other urinary system diseases such as urinary stones, urinary tract infections, etc.?
7. Have you recently engaged in extensive exercise or suffered muscle injuries?
8. Have you ever had any allergies? Have you recently come into contact with any allergens?
9. Have you ever used any medication that has kidney damage as a side effect for a long time? Which medication?
10. Have you ever been exposed to radiation, pesticides, heavy metals or other harmful substances?
11. Do you or any of your relatives suffer from hereditary kidney disease?
12. Do you have any other diseases that could cause kidney damage, such as hepatitis, hypertension, or diabetes? Are you taking medication to control these conditions?
13. Do you smoke? How long have you been smoking? How many cigarettes do you smoke per day?
14. Do you have a drinking habit? Have you consumed a lot of alcohol recently?
15. Do you have any other diseases such as heart disease?
What questions can patients ask their doctor?
1. What is the most likely cause of my proteinuria?
2. Is my condition serious? Can it be cured?
3. What tests do I need to do?
4. How should I proceed with treatment now? Do I need to be hospitalized?
5. Are there any risks with this treatment?
6. I have other diseases. Will this affect my treatment?
7. If taking medication, what are the usage, dosage and precautions of the medication?
8. What should I pay attention to after returning home?
9. Do I need follow-up examinations? How often?
examine
Scheduled inspection
The doctor will first examine the kidneys to gain a preliminary understanding of their condition. They may then conduct a systemic physical examination to identify any systemic pathologies. If necessary, they may also perform routine blood tests, urine tests, renal function tests, immunological tests, pathological biopsies, and renal imaging studies.
Physical examination
Doctors will first focus on the kidneys to check for any signs of tenderness or masses, and may then perform body scans to check for any abnormalities. A physical examination can often provide a preliminary diagnosis of the cause of proteinuria.
Laboratory tests
1. Routine blood test
By observing changes in blood cell counts, we can determine whether the body has any pathological changes such as inflammation or infection.
2. Urine test
Healthy adults excrete very little protein in their urine daily (approximately 30-130 mg), and conventional qualitative tests generally return negative results. When the protein concentration exceeds 100 mg/L or 150 mg/24 hours of urine, a qualitative protein test will be positive, indicating proteinuria. Furthermore, urine analysis can be used to determine the type of protein and the presence of red blood cells, casts, and other components to help determine the cause of proteinuria.
3. Renal function test
Serum creatinine measurement can reflect changes in renal function.
4. Immunological examination
This test helps diagnose infections, tumors, autoimmune diseases, and other conditions.
Imaging examinations
Imaging examinations such as ultrasound, CT, and MRI can help doctors understand whether there are lesions in the kidneys and other parts of the body, as well as the extent and severity of the lesions. This is of great significance for the diagnosis and identification of the cause of proteinuria.
Pathological examination
If necessary, kidney biopsy should be taken and sent for pathological examination to help diagnose the type of kidney lesions and assess the severity of the lesions.
diagnosis
Diagnostic principles
Doctors usually make a clinical diagnosis based on medical history, typical symptoms of foamy urine and corresponding test results (such as blood routine, urine, immunology or renal function tests), exclude pseudoproteinuria, and actively look for the cause of proteinuria.
Diagnostic basis
1. The doctor will first rule out pseudoproteinuria. If the urine is mixed with blood, pus, inflammatory or tumor secretions, menstrual blood, semen, prostatic fluid, lymph fluid, or medication, and the urine is left for a long time or cooled, a routine qualitative urine protein test may also test positive. After centrifugation or filtration, the qualitative protein test will turn negative. Once pseudoproteinuria caused by these factors has been ruled out, true proteinuria can be confirmed.
2. Determine the amount of protein in the urine, the composition of the urine protein, the selectivity and nature of the proteinuria through various laboratory tests.
3. Determine the disease causing proteinuria based on medical history, symptoms and signs, laboratory tests, and auxiliary examinations. Renal puncture biopsy may be performed if necessary.
Differential diagnosis
1. Differential diagnosis of non-renal proteinuria
(1) Functional proteinuria
It is primarily caused by increased glomerular filtration membrane permeability after strenuous physical labor or exercise, long-distance marches, fever, working in high temperatures, severe cold, mental stress, congestive heart failure, or a high-protein diet. It often occurs in healthy young people or adults. The 24-hour urine protein level is generally less than 0.5g and rarely exceeds 1g. The main component is albumin.
(2) Postural (or orthostatic) proteinuria
Its occurrence is closely related to changes in body position. Characterized by the absence of urine protein in prone position, proteinuria occurs in an upright position or when the spine is in an increased lordotic position. Quantitative 24-hour urine protein is generally less than 1g, indicating non-selective proteinuria.
2. Differential diagnosis of glomerular proteinuria
(1) Primary glomerular disease
① Nephrotic syndrome: Clinical manifestations include massive proteinuria (≥3.5g/L/24h) and hypoalbuminemia (≤30g/L), often accompanied by edema and hyperlipidemia. These manifestations are directly or indirectly related to the leakage of plasma albumin from the glomeruli into the urine, so the development of nephrotic syndrome indicates the presence of glomerular disease. Hypoalbuminemia and massive proteinuria are essential for the diagnosis of nephrotic syndrome. Nephrotic syndrome is a group of clinical syndromes caused by a variety of etiologies, pathologies, pathogenesis, and clinical diseases. Various types of primary glomerular diseases can cause nephrotic syndrome, and common pathological types include minimal change disease, mild change disease, mesangial proliferative glomerulonephritis, membranous nephropathy, membranoproliferative glomerulonephritis, and focal glomerulosclerosis.
② Acute post-streptococcal nephritis: This is a typical form of acute nephritic syndrome, commonly seen in children but also in adults and even the elderly. Onset occurs 1 to 4 weeks after the initial infection, typically 6 to 12 days for those with a common cold, and an average of 2 weeks after cutaneous β-hemolytic streptococcal infection. Onset is abrupt, with gross or microscopic hematuria, accompanied by proteinuria, red blood cell casts, oliguria, edema, and hypertension. It may be accompanied by varying degrees of azotemia and a marked decrease in serum complement. In patients with no history of renal disease, this is a self-limiting disease, though a rare condition can become chronic.
③ Rapidly progressive glomerulonephritis: Clinical manifestations resemble severe acute nephritis, but with a more rapid onset, including prominent oliguria, even anuria, and significant hematuria. Proteinuria, elevated blood pressure, severe hemolytic anemia, and hypoproteinemia may also occur. Renal function deteriorates rapidly, progressing to renal failure, azotemia, and even end-stage renal failure. Anti-basement membrane antibodies and antineutrophil cytoplasmic antibodies (ANCA) are frequently positive. While there are numerous etiologies, the predominant pathological type is crescentic glomerulonephritis.
④ IgA nephropathy: This disease is an immunopathological diagnosis and represents a group of disorders that share common immunopathological features, unrelated to systemic disease. It is characterized by the presence of mononuclear IgA or predominantly IgA immunoglobulins with C3, deposited in the glomerular mesangium in a clumpy or granular manner, accompanied by mesangial cell proliferation. Clinical manifestations include hematuria, proteinuria with or without microscopic hematuria, nephrotic syndrome, hypertension, chronic renal failure, and sometimes a rapidly progressive nephritic syndrome. Urinalysis reveals hematuria and/or proteinuria, with some or all red blood cell casts; serum IgA levels are elevated, while complement levels are normal. This disease should be differentiated from purpuric nephritis, non-IgA mesangial proliferative nephritis, and lupus nephritis.
(2) Secondary glomerular lesions
① Lupus nephritis: In addition to systemic multisystem involvement, clinical manifestations of nephritis primarily include varying degrees of proteinuria, hypertension, edema, and renal insufficiency, which must be differentiated from primary glomerulonephritis. Lupus nephritis is often accompanied by hemolytic anemia or pancytopenia, a significantly elevated erythrocyte sedimentation rate, positive antinuclear antibodies, anti-ds-DNA, and anti-sm antibodies, hypocomplementemia, and sometimes the presence of lupus cells in the blood. Urine protein is often >0.5g/24h, and heavy proteinuria may also occur, or clinical manifestations of secondary nephrotic syndrome may be present.
②Purpura nephritis: Henoch-Schönlein purpura is an allergic disease. When the kidneys are primarily affected, it is called purpura nephritis. Most kidney disease symptoms appear simultaneously with rash and arthritis. Hematuria and proteinuria may also appear several weeks after the rash appears. Only in a few cases will hematuria appear first, followed by rash, arthritis, etc. The clinical manifestations are similar to those of acute glomerulonephritis, mainly manifested as microscopic hematuria or intermittent gross hematuria. Proteinuria, hypertension, edema, and renal insufficiency may also occur in a few cases. Patients with severe proteinuria may have symptoms of nephrotic syndrome. Atypical cases should be differentiated from acute nephritis, lupus nephritis, IgA nephropathy, etc.
③ Diabetic nephropathy: often occurs 5 to 10 years after diabetes. Typical cases include polydipsia, polyphagia, polyuria, weight loss, and other diabetic microvascular damage. Urine protein quantification is >0.5g/24h. Severe cases manifest as nephrotic syndrome or even renal failure.
④ Renal amyloidosis: Amyloidosis is a rare systemic disease characterized by the deposition of amyloid deposits throughout various organs. The most common renal manifestation is proteinuria, which in most cases consists primarily of large, low-molecular-weight, low-selective proteins. The degree of proteinuria is proportional to the severity of glomerular lesions and can persist for several years, often misdiagnosed as glomerulitis. A definitive diagnosis requires a renal biopsy (Congo red stain positive). This condition should be considered in patients with unexplained proteinuria, adult nephrotic syndrome, bilateral kidney enlargement, chronic infection, rheumatoid arthritis with proteinuria, or proteinuria with anemia.
⑤ Hypertensive nephropathy: more common in the elderly, the incidence of hypertensive nephropathy is related to the severity of hypertension itself and the duration of the disease. The more severe the hypertension and the longer the course of the disease, the higher the incidence of hypertensive nephropathy and renal failure. The degree of renal artery sclerosis is parallel to that of retinal artery sclerosis, with increased nocturia first, followed by proteinuria. Arteriosclerosis has only mild proteinuria, casts, and very few red and white blood cells. Malignant nephrosclerosis has increased proteinuria, which may include red blood cell casts, a few hyaline casts, granular casts, and white blood cells. A small number of patients have gross hematuria or microscopic hematuria, and renal failure can occur rapidly.
⑥ Hepatitis B virus-associated nephritis: Circulating hepatitis B antigens can cause arthralgia, fever, polyangiitis, and glomerular disease. Clinically, in addition to hepatitis manifestations, there is also varying degrees of proteinuria, often accompanied by microscopic hematuria. Essential criteria for diagnosis are: positive serum hepatitis B antigen; the presence of immune complex nephritis; and the presence of hepatitis B antigen in renal tissue biopsies.
⑦ Kidney disease caused by circulatory disorders: Constrictive pericarditis, congestive heart failure, renal vein thrombosis, or inferior vena cava thrombosis can all cause renal venous circulatory disorders, resulting in elevated renal venous pressure and causing massive proteinuria, and even nephrotic syndrome. Renal vein thrombosis is the most common of these, and can manifest as acute low back pain, hematuria, proteinuria, and even nephrotic syndrome, oliguria, and acute renal failure.
⑧ Nephropathy caused by toxic conditions: Organic or inorganic mercury, organic gold, lithium, silver, arsenic, penicillamine, heroin, probenecid, nonsteroidal anti-inflammatory drugs, captopril, meptoin, warfarin, rifampicin, perchlorates, insecticides, contrast agents, and Chinese herbal medicines can cause kidney damage and proteinuria. The diagnosis can be confirmed based on medication use and a history of poisoning.
⑨ Kidney disease caused by malignant tumors: Various malignancies can cause glomerular damage, with adenocarcinomas of the lung, colon, stomach, and breast being the most common. Multiple myeloma, lymphoma, and leukemia can also cause glomerular damage. Glomerular damage caused by adenocarcinoma and Hodgkin’s disease primarily manifests as nephrotic syndrome. Kidney damage caused by tumors, in addition to glomerular involvement, can also cause uric acid nephropathy, hypercalcemic nephropathy, hypokalemic nephropathy, and obstructive nephropathy, which can progress to chronic renal failure. Some cancer patients may first develop kidney disease and then develop tumor symptoms, which should be of concern.
(3) Congenital glomerular disease
① Congenital nephrotic syndrome: This is an autosomal recessive genetic disorder that can be divided into two types: the Finnish type and the non-Finnish type. The Finnish type, which occurs more frequently in Finland, presents with proteinuria at birth or within the first week of life, progressing to severe nephrotic syndrome within three months of birth. The non-Finnish type develops slightly later than the Finnish type, often presenting with proteinuria in childhood. Nephrotic syndrome is milder and often accompanied by hypertension. Renal impairment progresses rapidly, and death from renal failure is common in childhood.
② Hereditary nephritis: This is an autosomal dominant genetic disorder, with Alport syndrome being the most common. It is also known as hereditary progressive nephritis or oculo-auriculorenal syndrome. Symptoms vary in severity, ranging from mild proteinuria to chronic renal failure. Key features include chronic renal damage, bilateral high-frequency sensorineural hearing loss, and ocular lesions such as cataracts, spherical lenses, corneal pigmentation, and retinal detachment. The earliest prominent manifestation is recurrent hematuria, with severe proteinuria occurring in 30% to 40% of cases. Red blood cells and red blood cell casts may be seen in the urine sediment. Hypertension may develop in the later stages. There is a strong family history, and it is more common in young men. It must be differentiated from benign familial hematuria.
Thin basement membrane nephropathy (TBM): Formerly known as benign familial hematuria, this condition is often inherited in an autosomal dominant manner, although it can also occur in families with autosomal recessive inheritance. TBM is diagnosed by electron microscopy, with the sole or most significant change being diffuse thinning of the GBM, with GBM thickness approximately 2/3 to 1/3 of normal. The vast majority of patients present with hematuria, with the majority experiencing persistent microscopic hematuria. Some adult patients also have mild proteinuria, and a minority present with mild proteinuria as the sole clinical manifestation.
④Fabry disease: also known as diffuse angiokeratoma and glycosphingolipid storage disease, it is a rare sex-linked dominant hereditary disorder of glycosphingolipid metabolism. Early manifestations include renal tubular dysfunction, including nephrogenic diabetes insipidus, renal tubular acidosis, or renal glycosuria. Renal involvement primarily manifests as mild proteinuria, occasionally accompanied by hematuria. Nephrotic syndrome is rare, with mild hypertension and slow decline in renal function. Urine sediment examination reveals birefringent fat bodies. Additionally, the disease may present with skin, nervous system, and cardiovascular lesions. Uremia develops in the late stages.
3. Differential diagnosis of tubular proteinuria
(1) Pyelonephritis
Symptoms of this disease include proteinuria, hematuria, and leukocyturia. Urine protein levels are low, often less than 1g, and the urine contains numerous white blood cells, including casts. Urine cultures are positive for pathogens and are effective with antibiotics. Acute cases are accompanied by fever and flank pain, while chronic cases may develop focal cortical scarring and deformation of the renal pelvis and calyces.
(2) Interstitial nephritis
① Acute interstitial nephritis: This disease is caused by acute systemic infection, drug allergy, or poisoning. Renal damage includes oliguria, proteinuria, hematuria, and cystic urine. Severe cases may lead to acute renal failure. Proteinuria is usually mild to moderate, and a renal biopsy is necessary for diagnosis.
Chronic interstitial nephritis: Mild proteinuria, with a quantitative level not exceeding 2g/24h, is characterized by low-molecular-weight proteinuria. There may be casts in the urine and varying degrees of red and white blood cells in the urine. There is also decreased renal concentrating function, increased nocturia, and decreased urine specific gravity and osmolality. Urine enzyme tests may be abnormal.
(3) Acute tubular necrosis
Caused by nephrotoxic substances or renal ischemia. The amount of urine protein is mild, and urine routine examination shows urine protein (+) to (++).
(4) Reflux nephropathy
This disease is a kidney disease caused by vesicoureteral and intrarenal reflux, resulting in kidney scarring and ultimately end-stage renal failure. Key clinical manifestations include recurrent urinary tract infections, proteinuria, hypertension, nocturia, and polyuria. Proteinuria may be the initial symptom, followed by a gradual increase, indicating progressive glomerular disease and a poor prognosis. Other common manifestations include infection, obstruction, microscopic and gross hematuria, and renal failure.
(5) Hyperuricemia nephropathy
① Acute hyperuricemic nephropathy: This disease presents with an abrupt onset. Patients with myeloma, lymphoproliferative disorders, or a history of chemotherapy or radiotherapy for malignant tumors experience massive cell destruction and hypermetabolism of nucleic acids, leading to acute hyperuricemia. Large amounts of uric acid or urate crystals precipitate within the renal interstitium or tubular lumen, resulting in renal obstruction and oliguric acute renal failure. Low to moderate amounts of proteinuria are present, accompanied by arthritis and urate urinary stones.
Gouty nephropathy: Chronic hyperuricemia is characterized by the accumulation of needle-shaped, birefringent urate crystals within the renal interstitium and tubules. Clinical manifestations include minimal to moderate proteinuria, the presence of red and white blood cells in the urine sediment, and decreased renal concentrating function. In later stages, the disease may involve the glomeruli and lead to renal insufficiency.
(6) Analgesic nephropathy
Analgesic nephropathy is a chronic kidney disease caused by long-term analgesic abuse. It is characterized by renal papillary necrosis and chronic interstitial nephritis. Necrotic papillary tissue may sometimes be excreted in the urine. Chronic renal insufficiency may also present with proteinuria (<1.0 g/24 hours), microscopic hematuria, tubular condensation, and decreased acidification.
(7) Renal tubular acidosis
This disease is a group of clinical syndromes caused by the reabsorption disorder of HCO3- in the proximal renal tubules or (and) the inability to establish a normal pH gradient between the blood and the tubular fluid in the distal renal tubules, manifested as metabolic acidosis, electrolyte imbalance, and in a few cases, low-molecular-weight, tubular proteinuria.
4. Differential diagnosis of overflow proteinuria
(1) Multiple myeloma
This disease is a malignant tumor characterized by abnormal proliferation of plasma cells. In addition to anemia, plasmacytosis, bone pain, osteolytic lesions, and pathological fractures, most patients present with isolated proteinuria, with varying degrees of proteinuria. A few also develop nephrotic syndrome. This proteinuria is predominantly composed of low-molecular-weight proteins, and the urine is positive for Bence Jones protein.
(2) Light chain disease and light chain deposition disease
Renal damage in this disease is primarily proteinuria or nephrotic syndrome, with hematuria rarely present. In severe cases, uremia may develop. Large amounts of monoclonal light chains can be found in the urine.
5. Tissue proteinuria
Abnormalities in tissue proteins and organ-specific antigens in urine can help identify and determine the site of disease. For example, myoglobin can be detected in cases of myocardial and skeletal muscle damage, hemoglobin can be detected in cases of hemolytic anemia, glomerular basement membrane antigens can be increased in the urine of patients with nephrotic syndrome, and related specific antigens can be detected in the urine of patients with cancer.
treat
Expected treatment
Physiological proteinuria does not require treatment and will gradually improve over time after the inducing factor is removed. Proteinuria caused by pathological factors can be treated individually based on the cause and severity of the condition.
Treatment
1. Diet therapy
To prevent excessive protein from leaking into the urine and causing vacuolar degeneration of the renal tubules, animal protein (high-quality protein) that is easily absorbed and utilized should be consumed.
2. Treatment of primary disease
Actively treat the primary disease, such as controlling blood sugar, infection, hypertension, and conducting anti-allergic treatment.
3. Drug treatment
(1) Angiotensin-converting enzyme inhibitors (ACEI) and angiotensin II receptor blockers (ARB)
Both can dilate the renal arteries, thereby reducing intraglomerular pressure, lowering filtration pressure, and reducing the permeability of the glomerular filtration membrane to proteins. They can also inhibit renal fibrosis, alleviate inflammation, and protect the kidneys. However, during medication, serum creatinine, blood pressure, and potassium levels should be closely monitored to prevent hypotension, prerenal oliguria, and hyperkalemia.
(2) Hormones
The proteinuria-lowering effect of glucocorticoids may be closely related to their immunosuppressive and anti-inflammatory mechanisms. Prednisone is the preferred drug. During treatment, attention should be paid to preventing and controlling infections and other adverse reactions.
(3) Cytotoxic drugs
Often used concurrently with hormones, it can reduce the duration and dosage of hormone therapy and minimize the risk of hormone side effects. It can affect different stages of biosynthesis, hindering cell division and proliferation, and suppressing the immune response, thereby reducing proteinuria. Commonly used drugs include cyclophosphamide (CTX), azathioprine, and cyclosporine A (CsA).
(4) Traditional Chinese Medicine
Tripterygium wilfordii polyglycosides can alter the charge state of the glomerular basement membrane and have immunomodulatory and anti-inflammatory effects, thereby preventing protein filtration. However, they should be used with caution in patients with infertility or renal insufficiency.
4. Other treatments
Anticoagulant and lipid-lowering therapy have certain effects on controlling proteinuria.
Related drugs
Prednisone, cyclophosphamide (CTX), azathioprine, cyclosporine A (CsA), tripterygium wilfordii glycosides
Prognosis
General prognosisProteinuria caused by physiological factors is temporary and returns to normal after the cause is removed. The prognosis of proteinuria caused by pathological factors is related to the primary disease.
Self-healingProteinuria caused by physiological factors can heal itself after the inducement is removed.
daily
Nursing principles
In daily life, you need to take medication as prescribed by the doctor, eat a balanced diet, avoid excessive fatigue, and actively cooperate with the doctor for treatment.
Psychological careDue to the lack of understanding of urinary protein, it is easy to cause negative emotions such as excessive worry, anxiety, irritability, and uneasiness. Patients can eliminate negative emotions and stabilize their mentality by listening to music or talking to others. At the same time, they can also learn about the relevant knowledge of urinary protein, understand its treatment methods, build confidence in treatment, and actively cooperate with the doctor’s treatment.
Medication careFollow the doctor’s instructions and use the medication correctly. Absolutely avoid stopping or adjusting the medication without authorization. Understand the medication usage, dosage, precautions and adverse reactions. If you feel unwell, inform the doctor in time so that the doctor can adjust the medication to prevent delays in treatment.
Life Management
1. Rest in a quiet and comfortable environment, maintain a regular schedule, ensure sleep, and avoid overwork.
2. Appropriately increasing physical exercise can help strengthen physical fitness, improve immunity and promote recovery.
diet
Dietary adjustmentA scientific and reasonable diet can enhance the therapeutic effect and promote recovery from the disease.
Dietary recommendations
Ensure nutritional supply, eat a low-salt, light diet, eat more foods rich in high-quality protein, vitamins, dietary fiber and other nutrients, and drink appropriate amounts of water every day.
Dietary taboosEat less greasy, spicy and irritating food, avoid pickled products, quit smoking and drinking to reduce the burden on the kidneys.