low molecular weight proteinuria
Introduction
Introduction Low-molecular proteinuria: Due to the filtration of glomerular filtration membrane and the reabsorption of renal tubules, the amount of protein in the urine of healthy people (multiple molecular weight proteins) is very small (less than 150 mg per day) ), when the protein is qualitatively tested, it is negative. Due to tubular dysfunction, the protein that has been filtered through normal glomeruli is reabsorbed. Low molecular proteins generally refer to proteins with a molecular weight of 40,000 d. Because renal tubules play an important role in the reabsorption and catabolism of low molecular proteins, low molecular proteinuria excretion increases in renal tubular lesions.
Cause
Cause
1. Dent disease: is an X-linked hereditary tubular disease. First reported in the UK. The disease is characterized by low molecular proteinuria, hypercalciuria, renal calcification, and kidney stones, but the uric acid function is normal. Some patients have rickets and progressive renal failure, while urinary growth hormone excretion levels are high. Renal pathology showed mild mesangial proliferation and minor lesions in the tubules. Male onset, female carrying. Female carriers have low molecular proteinuria, and half have high calcium urine but no obvious symptoms.
2. X-linked recessive inherited nephrolithiasis: a disease characterized by proximal tubule dysfunction. First reported in North America. Male onset, female carrying. Women often have mild urinalysis abnormalities, varying degrees of low molecular proteinuria, and 1/3 of patients have hypercalciuria. Patients often have proteinuria and microscopic hematuria within 1 year of age, and kidney stones appear in 3-6 years of age. There are also patients who have developed symptoms during adolescence. Clinical manifestations are kidney stones, renal calcification and progressive renal failure. Stones often consist of calcium oxalate and calcium phosphate. Not all patients develop to renal failure. Kidney transplantation is effective, suggesting that the disease is tubular rather than systemic. There were 1 case of rickets in 30 children. Kidney pathology showed small ball sclerosis, interstitial fibrosis and tubule atrophy.
3. Low molecular proteinuria with hypercalciuria and renal calcification: first reported in Japan. The patient is often a male patient in a family. Such patients have low molecular proteinuria, hypercalciuria, renal calcification, and urinary concentrating dysfunction. Lack of renal colic and rickets is not a distinguishing point from XRN and Dent. However, renal calcification at 3-5 years indicates a poor prognosis. Urinary screening of school-age children and preschool children in Japan found that asymptomatic patients younger than 14 years old were mostly normal.
4. X-linked recessive hypophosphatemic rickets: first discovered in a family in Italy. Male patients in this family are characterized by rickets, osteomalacia, hypophosphatemia, renal calcification, and early progressive renal failure. They differ from X-linked phenotypic hereditary hemolytic rickets, which have high calciumuria, 1,25(OH)2D elevation, and proteinuria, as well as renal calcification and progression to renal failure. Male onset, female carrying. Female carriers were normal except for hypercalciuria. In terms of treatment, it is generally advocated that the intake of sodium in the diet should be restricted, and the diet containing more oxalic acid should be restricted. The formation of crystallization by oxalate can further promote the formation of stones. Absorptive idiopathic hypercalciuria should avoid excessive calcium intake or taking phosphate, especially for those with hypophosphatemia. Renal hypercalciuria is not affected by dietary calcium intake. Thiazide diuretics promote calcium reabsorption in the distal tubules and lower urinary calcium. Amiloride (amperidose) also promotes the reabsorption of calcium by the renal tubules and inhibits the excretion of potassium. The mechanism is unknown. It can be combined with a thiazide diuretic in addition to its application. Attention should be paid to electrolyte imbalance when applying these drugs. Kidney transplantation can be performed in patients with end-stage renal failure.
Examine
an examination
Related inspection
Urine sediment urine sediment tubular urine sediment type urine protein urine glutamicum transferase
Low-molecular protein in urine accounts for about 70%, while albumin only accounts for 15-25%. Urine protein is generally quantified at 1g/24h, rarely exceeding 2g/24h.
The following diagnostics can be used to assist in the diagnosis:
1, urine protein clearance rate.
2. Selective protein index.
3, urine sediment tube type inspection.
4, urine protein examination.
5, qualitative test of urinary acid.
Diagnosis is based on medical history, clinical manifestations, and examination.
Diagnosis
Differential diagnosis
1, acute glomerulonephritis: after streptococcal infection, edema, hypertension, hematuria, proteinuria and tubular urine.
2, chronic glomerulonephritis: edema from the lower extremity, spread from the bottom up, long course of disease, easy to relapse, late stage often have renal dysfunction, the first appearance of hypertension.
3, pyelonephritis: systemic infection symptoms, low back pain, bladder irritation, laboratory tests for pyuria urine is its characteristics.
4, systemic lupus erythematosus: belonging to autoimmune diseases, hair loss, facial butterfly erythema, oral ulcers, migratory arthritis, photoallergies, Raynaud's phenomenon, multiple organ damage, especially heart and kidney, especially kidney Loss first. Its proteinuria is generally more, and some patients appear in the form of nephrotic syndrome.
5, multiple myeloma: elderly men with good hair, anemia and is not commensurate with kidney damage. The disease progresses rapidly and is easy to damage kidney function, bone destruction, bone pain, and pathological fracture. Its urine protein is spilled proteinuria.
6, other: severe exercise, microalbuminuria, fever, proteinuria, heart failure, renal congestion caused by proteinuria, drug poisoning caused by proteinuria, due to a clear history and corresponding physical examination, the general diagnosis is not difficult.
