What Is a Juxtaglomerular Cell?

The glomerulus is a blood filter. The capillary wall of the glomerulus forms a filter membrane. When circulating blood passes through the glomerular capillaries, water and small molecule solutes in the plasma, including a small amount of small-molecular-weight plasma proteins, can be filtered into the cystic cavity of the renal capsule to form a filtrate, which is proved by micropuncture experiments The glomerular filtrate is the ultrafiltrate in the plasma.

Glomerulus

The glomerulus is a blood filter. The capillary wall of the glomerulus forms a filter membrane. As circulating blood passes through the glomerular capillaries, water and small molecule solutes in the plasma, including small amounts of smaller molecular weight

Micro-piercing method uses micromanipulator to insert fine glass with outer diameter of 6-10 m into the cystic cavity of renal corpuscle. Paraffin oil is injected into the proximal tubule at the junction with the capsule cavity to prevent the filtrate from entering the renal tubule. Micro-chemical analysis of the liquid drawn directly into the cavity of the capsule using a micro-glass tube (Figure 8-2). Analysis shows that in addition to the low protein content, various crystalline substances such as glucose,

The glomerular filtration rate refers to the amount of filtrate produced by the two kidneys per unit time, which is about 125 ml / min in normal adults. The ratio of glomerular filtration rate to renal plasma flow is called

filter

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In the late 1920s, a micro-piercing technique was developed. This technique uses a thin glass tube with a diameter of 7 to 15 to insert into the glomerulus of an amphibian (frog or tadpole) or mammal (rat or guinea pig) kidney ( Figure 10-5), extract the cyst fluid for analysis. Analysis of this type of sac fluid shows that it meets the characteristics of ultrafiltration:

The filtrate (raw urine) contains only a very small amount of protein;

The filtrate (raw urine) mainly contains small molecules or ions, such as glucose,

Glomerular profile

Glomerular disease (commonly referred to as nephritis, but not exactly) is not a single disease, but a group of diseases with different pathological types and often overlapping clinical manifestations caused by multiple etiology and pathogenesis.

Glomerular classification principle

The classification of glomerular diseases has the following principles:

Classification according to clinical manifestations;

Change typing according to function;

typing according to the anatomical part of the lesion;

typing according to pathological morphology;

type according to the pathogenesis;

Type according to the cause.

The latter two must be based on a deep understanding of the nature of the disease and are more difficult to achieve. Pathological typing must depend on biopsy and pathological examination. Therefore, clinical and functional classification is not only necessary for the majority of primary hospitals in China to carry out the clinical treatment of glomerular diseases, but also a diagnostic method necessary for the clinical work of renal diseases in any country and any medical level. Abolished.

Characteristics of glomerular disease

Those with the following clinical characteristics are glomerular diseases:

Glomerular proteinuria (mainly albumin) with cast urine and / or glomerular hematuria;

Extrarenal manifestations are hypertension and edema;

The impairment of glomerular filtration function precedes and is more important than renal tubular dysfunction.

Chronic glomerulonephritis

Chronic glomerulonephritis (chronic glomerulonephritis), referred to as chronic nephritis, refers to the basic clinical manifestations of proteinuria, hematuria, hypertension, and edema. The onset methods are different, the disease is prolonged, the disease progresses slowly, and renal function can be varied Decreased, eventually developing into a group of glomerulopathy of chronic renal failure. Due to the different pathological types and stages of the disease in this group, the main clinical manifestations are different, and the disease manifestations are diverse.

Clinical symptoms:

Chronic nephritis is a group of glomerular diseases with diverse etiology and different pathological forms, and similar clinical manifestations. Their common manifestations are edema, hypertension and abnormal changes in urine.

Edema: During the whole course of the disease, most patients will have varying degrees of edema. The degree of edema can be mild or severe. Those who are milder can only find swelling around the orbit, face, or edema in the lower limbs and ankles in the afternoon after waking up. In severe patients, systemic edema may occur. However, there are very few patients who do not appear edema throughout the course of the disease and are often easily ignored.

Hypertension: Some patients come to the hospital for treatment of high blood pressure symptoms. Doctors need to test their urine before they know that the blood pressure is caused by chronic nephritis. For patients with chronic nephritis, the occurrence of hypertension is a sooner or later process. The increase in blood pressure can be continuous or intermittent, and it is characterized by an increase in diastolic blood pressure (higher than 12.7 kPa). The degree also varies greatly from individual to individual, only 18.7-21.3 / 12.7-13.3kPa in the light, and even more severe than 26.7 / 14.7kPa in the severe.

abnormal changes in urine: abnormal urine is almost a necessary phenomenon in patients with chronic nephritis, including changes in urine volume and abnormalities in microscopy. There is a decrease in urine output in patients with edema, and the heavier the edema is, the more obvious the decrease in urine output. Most patients without edema have normal urine output. When the patient's kidney is severely damaged, and the urine's concentration-dilution function is impaired, there will also be an increase in nocturia and a decrease in urine specific gravity. When the urine of patients with chronic nephritis is observed under a microscope, it can be found that almost all patients have proteinuria, and the urine protein content ranges from (±) to (++++). Red blood cells, white blood cells, granular casts, and clear casts can be seen in urine sediments to varying degrees. When an acute attack occurs, there can be significant hematuria, and even gross hematuria. In addition, patients with chronic nephritis will experience clinical symptoms such as dizziness, insomnia, poor fatigue, intolerance to fatigue, and varying degrees of anemia.

Diagnostic criteria:

1. Slow onset, prolonged illness, mild to severe, renal function gradually decline, anemia, electrolyte disorders, blood urea nitrogen, serum creatinine and other conditions may appear in the later stage.

2. There are manifestations of proteinuria, hematuria, edema, and hypertension.

3 During the course of the disease, acute attacks can be induced due to respiratory infections and other reasons, and symptoms similar to acute nephritis appear, and some cases may have an automatic remission period.

Treatment measures:

First, the general treatment of patients without obvious edema, hypertension, hematuria and proteinuria is not serious, no renal insufficiency manifestations, can take care of themselves, and can even engage in light labor, but to prevent respiratory infections, avoid fatigue, do not use toxic effects on the kidney Drug. Patients with significant hypertension, edema, or those with short-term renal dysfunction should stay in bed and limit the intake of salt to 2 to 3 g. For those who have lost a lot of protein in the urine and have acceptable kidney function, it is advisable to add animal proteins with high bioavailability, such as eggs, milk, fish, lean meat, etc., and those who already have impaired kidney function (endogenous creatinine clearance rate is 30ml / min), the amount of protein should be limited to about 30g, and if necessary, an appropriate amount of essential amino acids should be added orally.

Two hormones, immunosuppressants. Due to repetitive and strong side effects, more and more people are rejecting therapeutic drugs and new treatments for chronic nephritis are needed)

Three pairs of azotemia treatment

People who have azotemia in the short term or appear for the first time, or have a recent increase should be bed rest and restrict excessive activities.

Diet and nutrition For those without obvious edema and hypertension, it is not necessary to limit the intake of water and sodium salts. It is important to increase the amount of water to increase urine output. It is not necessary to limit protein intake for patients with mild to moderate azotemia to maintain a positive nitrogen balance in the body, especially for patients who lose more protein every day. For a large amount of proteinuria with mild azotemia can increase plant protein such as soybeans. Patients with severe azotemia or recent progressive azotemia should appropriately limit protein intake.

About urine output and urine osmotic concentration Generally, the urine osmotic concentration of patients with chronic nephritis azotemia is usually 400mOsm / L or less. If the daily urine output is only 1L, it is not enough to discharge nitrogen-containing solutes, so the urine output should be 1.5L. Or above, appropriate drinking water or light tea can achieve this purpose, and intermittently taking diuretics if necessary.

Control of hypertension Chronic nephritis azotemia and renal parenchymal hypertension often indicate a poor prognosis, and persistent or severe renal hypertension can aggravate azotemia. Although the use of general antihypertensive drugs can reduce peripheral vascular resistance, it does not necessarily reduce glomerular vascular resistance. Increased glomerular resistance in and out of the arterioles reduces glomerular filtration. Whether calcium channel blockers such as nifedipine can reduce intraglomerular pressure and protect renal function is still questioned. It is now recognized that angiotensin-converting enzyme inhibitors not only reduce peripheral vascular resistance, but also inhibit renin in tissues. The angiotensin system can reduce the tension of the glomeruli and efferent arteries and improve the hemodynamic changes in the glomeruli. ACEI can still reduce the degradation of bradykinin in the tissue and enhance the effect of bradykinin expansion. Bradykinin can still stimulate cell membrane phospholipids to release arachidonic acid, promote prostaglandin production and enhance the effect of vasodilation. ACEI still inhibits the effect of angiotensin on glomerular mesangial cells. These mechanisms of action are reflected in the kidney tissue and can improve hemodynamics in the glomerulus. For patients with moderate to severe hypertension and cardiac hypertrophy, the use of ACEI can still reduce or inhibit the effect of angiotensin on myocardial hyperplasia and hypertrophy of vascular smooth muscle and thickening of the middle wall of blood vessels. This can prevent the thickening of blood vessels and Hypertrophy of myocardial cells is very helpful. However, ACEI causes a decrease in glomerular arteriolar arteriolar tension, which can sometimes reduce GFR. Therefore, ACEI should not be used in excessive doses in azotemia, and renal function should be closely monitored, and potassium-sparing diuretics should not be used to prevent it. Hyperkalemia. Commonly used drugs are captopril 12.5 to 25 mg once, 2 to 3 times daily; or benazepril (lotinxin) 1 to 2 times daily, 10 mg each time, or enalapril 10 mg, 1 daily Times. Or cinapril 2.5 ~ 5mg once a day, benazepril, cinapril, and enalapril are long-acting ACEI, if you cannot control hypertension, you can add amlodipine (Luohuxi) 5 ~ 10mg 1 to 2 times daily.

Treatment of azotemia during the treatment of nephrotic syndrome GFR often decreases to varying degrees in chronic nephritis nephropathy edema phase and edema resolution phase.

It is related to the following factors:

Degree of pathologically active lesions;

renal interstitial edema;

decreased glomerular ultrafiltration coefficient;

Blood volume decreases (7% to 38% of cases);

A large amount of hormone application causes high catabolism in the body;

Application of drugs that are harmful to the kidneys;

Interstitial nephritis;

Renal vein thrombosis.

It is often difficult to determine the cause in a timely manner. Except for items , , and , which must be dealt with in a timely manner, if there is no infection, sometimes you need to wait patiently and not be overly active; combined with acute interstitial nephritis, whether it is the immune response of the disease itself, Drug allergic reactions using short-range and high-dose hormones can often reduce azotemia and should be treated in a timely manner.

Anticoagulation in our hospital for more than 400 cases of various pathological types of glomerulonephritis with hypercoagulable state and fibrinoid necrosis in the kidney combined with heparin 50 80mg / day and urokinase 2 80,000 u / d intravenous drip In the treatment of 2 to 8 weeks, renal function often improved to varying degrees, and no severe bleeding occurred. For patients with refractory or refractory renal venous thrombosis, renal arterial and venous intubation technology has been used to inject 200,000 u of urokinase to achieve good results in renal venous thrombosis.

Management of hyperuricemia A small number of patients with chronic nephritis azotemia complicated by hyperuricemia. The increase in blood uric acid is not proportional to the decrease in endogenous creatinine clearance, indicating that hyperuricemia is not the result of azotemia. The use of allopurinol to reduce blood uric acid can improve renal function, but the dose should be small and the duration of medication should be short. Reduce your medicine fast. Drugs that increase uric acid excretion should not be used.

In other glomerulonephritis, inflammatory cells infiltrated in renal tissue can produce a large number of oxygen free radicals. Glomerular mesangial cells are also stimulated by immune complexes, membrane attack complexes and platelet activating factors to produce reactive oxygen species. Oxygen free radicals can directly damage or destroy glomerular basement membrane and epithelial cells through membrane lipid peroxidation. In addition, many patients with glomerular disease have low antioxidant capacity, which is manifested by reduced blood antioxidant enzymes such as serum superoxide dismutase and reduced antioxidants such as vitamins B2, E, and zinc and selenium. Therefore, how to inhibit the production of oxygen free radicals in kidney tissues, whether to use antioxidants and which antioxidants are good are worth further observation and accumulated experience. Chronic nephritis nephrotic syndrome is often accompanied by varying degrees of hyperlipidemia. It is known that hypercholesterolemia, especially low-density lipoprotein changes, can cause the production of lipid peroxides in renal tissues, and accelerate glomerular sclerosis and tubular damage. Increasing blood albumin levels can reduce blood lipid levels.

In short, patients with chronic nephritis azotemia are standing at the crossroads towards chronic renal failure or stable disease. Care should be taken to find the cause of short-term progressive azotemia or the first occurrence of azotemia. Do not simply think of it as the stage of development of chronic nephritis. In many cases, good renal function can be maintained for a long period of time after removing the predisposing factors.