What is renal parenchymal hypertension?

What is renal parenchyma? The renal parenchyma can be divided into cortex and medulla, and the cortex is composed of glomeruli and curved tubules. The medulla is composed of 15 to 20 kidney vertebral bodies, and the tip of the kidney cone protrudes into the renal nipple, which is the opening of the nipple tube and the collecting tube. The renal pelvis is funnel-shaped, surrounding 1~3 kidney nipples, and every 2~3 kidneys are combined into one kidney sputum. Generally, the kidney has 3 large sputum, called upper, middle and lower sac, or only there are two big cockroaches. Daxie is synthesized into renal pelvis. Most of the renal pelvis is located in the renal parenchyma, which is called the intrarenal pyelone. Most of it is located outside the renal parenchyma.

Renal substantial hypertension

What is a renal parenchymal disease? It refers to the lesion of the kidney. Such as: substantial kidney hypertension.

Renal parenchymal hypertension refers to an increase in blood pressure in patients due to substantial renal lesions and renal artery disease. In general, more than 90% of patients with renal failure are associated with varying degrees of hypertension. Renal substantial hypertension is a type of secondary hypertension. The clinical symptoms often show that about half of them can hear continuous vasoconstrictory murmurs at specific sites; the course is short, the progress is fast, and the diastolic phase is often accompanied by back pain, no response to drug treatment; symptoms are mostly present before 30 years old or after 50 years old, with sudden or long-term high blood pressure suddenly increasing.

Renal hypertension symptoms

Compared with the same level of essential hypertension, renal parenchymal hypertension is more likely to progress to malignant hypertension than primary hypertension, and the incidence rate is about 2 times higher than that of the latter. Among them, IgA nephropathy, especially hyperplasia or sclerosing IgA nephropathy secondary to malignant hypertension is particularly common. Moreover, compared with primary malignant hypertension, the prognosis of renal malignant hypertension is even worse. According to the authors, the former has a kidney survival rate of 60% in 5 years, while the latter has a kidney survival rate of only 4% in one and a half years.

Fundus lesions of renal parenchymal hypertension are often severe, and cardiac and cerebrovascular complications are often more likely to occur. This is because in addition to hypertension, renal parenchymal disease often has other complex cardiovascular risk factors, such as lipid metabolism disorder in nephrotic syndrome, glucose metabolism disorder in diabetic nephropathy, anemia in renal insufficiency, hyperuricemia symptoms, hyperhomocysteinemia, uremic toxins, metabolic acidosis, and microinflammation, these combined factors will significantly increase the incidence of cardiovascular complications.

Here, special emphasis should be placed on the effects of renal hypertension on the progression of basic kidney disease, especially chronic glomerular disease. In chronic glomerular disease, the anterior glomerular arteriole is in a diastolic state. Systemic hypertension is easily transmitted to the glomerulus, causing glomerular hypertension, hyperperfusion and high filtration. This “three highs” can accelerate the survival. Glomerulosclerosis; at the same time, long-term hypertension can lead to small arteriosclerosis of the kidney, including vitreous changes in the arterioles of the afferents, thickening of the interlobular arteries and the endothelium of the arcuate arteries, narrowing the lumen of the arterioles secondary renal ischemia damage (glomerular ischemic contraction to ischemic sclerosis, tubular atrophy and renal interstitial fibrosis). Therefore, renal hypertension that is not well controlled will significantly accelerate the progression of renal parenchymal disease and form a vicious circle.

The glomerular disease with a large amount of urinary protein and the renal damage of hypertension are more obvious because the effects of the two are superimposed. It is known that proteinuria, especially large amounts of proteinuria, can cause glomerular hypertension, hyperperfusion and hyperfiltration to promote glomerular sclerosis; and, filtered proteins (including complement and growth factors, etc.) and protein-binding Certain substances (including lipids and iron) are reabsorbed by the renal tubules to activate tubular cells and release pathogenic factors (such as transforming growth factor beta) to promote renal interstitial fibrosis. Therefore, in patients with renal hypertensive patients with proteinuria, it is necessary to strictly control hypertension.

Pathological reasons:

A variety of renal parenchymal diseases can cause high blood pressure, and the incidence of hypertension in different renal parenchymal diseases is different.

  1. Unilateral renal parenchymal diseases that can cause hypertension include reflux nephropathy, chronic pyelonephritis, hydronephrosis and renal adenocarcinoma. If the test shows that the renal venous blood renin level is high, it is possible to remove the kidney early. Heal or significantly improve high blood pressure. Hypertension is more common in patients with congenital single kidney deficiency (renal non-development), and acquired single nephrectomy (removal of kidney or donor kidney) does not increase the risk of hypertension, and the mechanism is unclear.
  2. There are many bilateral renal parenchymal diseases that can cause hypertension, including primary and secondary glomerular diseases, chronic interstitial nephritis, and adult polycystic kidney disease. In general, the incidence of hypertension in primary and secondary glomerular diseases is higher than that in chronic interstitial nephritis and adult polycystic kidney disease. In primary and secondary glomerular diseases, pathology is proliferating and/or hardening. The highest incidence of hypertension in the performers. In addition, regardless of which kidney disease occurs when renal function damage occurs, the incidence of hypertension increases. According to the literature, about 90% of patients with end-stage renal disease have hypertension.

Disease diagnosis:

Renal substantial hypertension needs to be differentiated from renal vascular hypertension, renal lesions secondary to hypertension, and other secondary hypertension. Some patients have latent symptoms of kidney disease, and hypertension is very prominent and easily misdiagnosed as essential hypertension.

  1. Renal vascular hypertension:hypertension caused by unilateral or bilateral renal artery trunk or branch stenosis caused by various reasons, common causes are arteritis, fibromuscular dysplasia and atherosclerosis. If there is high blood pressure with the following clinical features, the disease should be suspected: patients who are under 30 years old or over 50 years old have no family history of hypertension; the course of hypertension is short and progresses rapidly, most of them show malignant hypertension; the retina may have Bleeding, exudation, optic disc edema, etc.; vocal murmurs can be heard in the head and neck, upper abdomen and/or lower back ridge area; X-ray and B-ultrasound examinations show differences in size and density of kidneys; renal venous blood test kidneys The activity of the hormone was increased, and the captopril (caprolactam) was positive for the renal chromatogram. Abdominal aorta or selective renal angiography with vascular stenosis can confirm the diagnosis.
  2. Hypertensive kidney disease:Renal substantial hypertension and primary hypertension secondary to renal damage identification, history is very important for its identification. Is high blood pressure first, or proteinuria first, plays a key role in differential diagnosis, the latter diagnosis points are as follows: amore than middle age, more common, may have a family history of hypertension; b before the occurrence of kidney damage has been more than 10 years Hypertension; c slow progression of the disease, tubular dysfunction (decreased urinary function, increased nocturia) earlier than glomerular dysfunction; d mild urine changes (low urine protein, less urinary microscopy); e often accompanied by hypertensive retinopathy, heart and brain complications; f diagnosis of this disease still need to exclude a variety of primary and secondary kidney disease. Renal biopsy is feasible when clinical diagnosis is difficult. Renal tissue pathology is helpful for differential diagnosis.
  3. Other secondary hypertension: 1 Endocrine hypertension: hypercortical hyperemia occurs in endocrine disorders such as hypercortisolism, pheochromocytoma, primary aldosteronism, hyperthyroidism, and menopause. Corresponding diagnosis can be made according to the endocrine history, special clinical manifestations and endocrine test. 2 aortic coarctation, congenital aortic coarctation or multiple arteritis caused by descending aorta and abdominal aortic stenosis, can lead to high blood pressure. Clinical features often have high blood pressure in the upper limbs and low blood pressure in the lower limbs; the abdominal aorta, femoral artery and other lower extremity arteries are weakened or inaccessible; the interscapular region, the ankle and the middle and upper abdomen may have pulsation of the collateral circulation artery. , tremors and murmurs; signs of left ventricular hypertrophy and dilatation. 3 craniocerebral lesions: some encephalitis or tumor, intracranial hypertension and other common hypertension, the neurological manifestations of this type of lesions are more characteristic, the diagnosis is generally not difficult. 4 pregnancy-induced hypertension syndrome: more than 3 to 4 months after the third trimester of pregnancy, childbirth or 48 hours after delivery, characterized by high blood pressure, edema and proteinuria, severe convulsions and coma.