How is acute tubulointerstitial nephritis diagnosed

Can you take traditional Chinese medicine for acute tubulointerstitial nephritis**Hello Yao Xintai; You can take traditional Chinese medicine, Chinese medicine syndrome differentiation treatment, I wish you a speed**.

Can acute tubulointerstitial nephritis be cured? Will there be any sequelae? Person: Qing Lengyuan 1 to remove the trigger in time 2Timely and positive**3Theoretically, it can be cured without sequelae.

Pathological changes: macroscopic observation: the kidney is enlarged, red, smooth surface, tense membrane, thickened cortex on the incision surface, and clear cortex medulla, which is called big red kidney; If there is a small punctate bleeding, it is also called a flea biting kidney.

Microscopic observation: (1) Globulus glomeria: capillary endothelial cells and mesangial cells are obviously proliferated and enlarged, and neutrophils and macrophages infiltrate the glomerular sac cavity and exudate inflammatory cells and cellulose, and red blood cells can also be seen.

2) Renal tubule: Epithelial cell edema, various casts formed by proteins, white blood cells, red blood cells and exfoliated epithelial cells appear in the lumen. (3) Interstitium:

hyperemia, edema, and a small number of inflammatory cells infiltrate the high grip.

Interstitial nephritis, also known as tubulointerstitial nephritis, is a clinicopathological syndrome of acute and chronic damage to the renal tubulointerstitial caused by various causes. Clinically, it is often divided into acute interstitial nephritis and chronic interstitial nephritis. Acute interstitial nephritis is characterized by a variety of causes of renal interstitial inflammatory cell infiltration, interstitial edema, and varying degrees of renal tubular damage with renal insufficiency.

The pathological manifestations of chronic interstitial nephritis are characterized by renal interstitial fibrosis, interstitial mononuclear cell infiltration, and tubular atrophy.

Acute tubular necrosis (ATN) is the most common type of acute renal failure, which is a clinical syndrome caused by renal tissue ischemia and toxic damage caused by renal tubular epithelial cell damage and necrosis, resulting in a sharp decrease in glomerular filtration rate (GFR), which is generally manifested as progressive azotemia, water-electrolyte and acid-base imbalance and a series of related symptoms, patients with moderate to severe acute tubular necrosis not only have severe renal failure, but also often have one or more complications, Sometimes it can be life-threatening and requires prompt and active rescue and resuscitation.

As the kidneys have lost their function, doctors will temporarily use dialysis** (commonly known as dialysis) to help remove toxins and waste products from the body. Patients with acute renal failure who have not been properly given ** or are uncontrollable to progress from acute to chronic renal failure must undergo lifelong dialysis due to uremia.

Dialysis is the process of selectively removing certain substances from the blood through filtration. That is to say, the toxic waste, water and salt accumulated in the patient's body after kidney failure are removed through artificial means, so that the patient's physical condition can be restored to a healthy state. There are two types of dialysis currently used:

Hemodialysis and peritoneal dialysis. Hemodialysis is the function of replacing the kidneys with a special machine. Peritoneal dialysis uses the body's peritoneum as a filter to remove toxins from the body.

Chapter 14 of the Clinical Super Book of Urology 02 Glomerular Diseases 03 Rapidly Progressive Glomerulonephritis: Concept, Pathological Classification, Diagnosis, and Principles.

Pathological changes: Light microscopy: proximal convoluted tubular epithelial cell steatosis.

The glomeruli are normal. Electron microscopy field excitation: extensive glomerular visceral epithelial cell fusion.

Immunopathology: negative. Clinical manifestations:

Males are more common in women, more common in children, typical manifestations of nephrotic syndrome, that is, massive proteinuria (>), hypoalbuminemia (<30g L), obvious edema and hyperlipidemia, only about 15% of patients are accompanied by microscopic hematuria, no persistent hypertension and decreased renal function like a sock.

a.Mesangial cells are markedly hyperglycerous.

b.The epithelial cells in the parietal layer of the balloon proliferate markedly to form crescents.

c.The diffuse nature of the basement membrane is significantly thickened.

d.Massive fibrosis of the glomeruli and vitreous.

e.There is a hump-like immune complex deposition on the lateral side of the basement membrane.

Correct answer: B

Answer] :d Analysis: Select D for this question.

Rapidly progressive glomerulonephritis is characterized by acute nephritis syndrome, rapid deterioration of renal function, and early onset of oliguric acute renal failure. The pathological type is crescent nephronephritis. This is because:

Under light microscopy, the main feature is the formation of a large crescent in the extensive (50) glomerular sac cavity (accounting for more than 50 of the glomerular sac cavity), and the early stage of the lesion is a cellular crescent and the later stage is a fibrous crescent. Master the knowledge points of "common **, diagnosis and differential diagnosis of rapidly progressive glomerulonephritis".