Renal parenchymal hypertension
Introduction
Introduction to renal parenchymal hypertension Renal parenchymal hypertension (renalparenchymalhypertension) is caused by various renal parenchymal diseases, accounting for 5% to 10% of all hypertension, the incidence of which is second only to essential hypertension, in secondary hypertension first place. basic knowledge The proportion of illness: mostly occurs in patients with nephritis, the incidence rate is about 0.003% - 0.006% Susceptible people: no special people Mode of infection: non-infectious Complications: renal failure, hypertensive encephalopathy
Cause
Kidney substantial hypertension cause
Unilateral renal parenchymal disease (25%) that can cause hypertension:
Including reflux nephropathy, chronic pyelonephritis, hydronephrosis and renal adenocarcinoma, if the test shows that the renal venous blood renin level is high, early resection of the kidney may cure or significantly improve high blood pressure, congenital single kidney deficiency For example, patients with hypertension (renal development) are more common, and acquired single nephrectomy (removal of kidney or transplant donor) does not increase the risk of hypertension, and the mechanism is unclear.
Bilateral renal parenchymal disease (30%) that causes high blood pressure:
Including primary, secondary glomerular disease, chronic interstitial nephritis, adult polycystic kidney disease, etc. In general, the incidence of hypertension in the original, secondary glomerular disease is higher than chronic interstitial nephritis and adults Type polycystic kidney disease, in the original, secondary glomerular disease, the pathological proliferation and / or hardening performance of the highest incidence of hypertension, in addition, regardless of which kidney disease occurs when renal damage occurs, the incidence of hypertension The rate has increased. According to the literature, about 90% of patients with end-stage renal disease have high blood pressure.
Factors that cause sodium retention and increased blood volume (20%):
(1) lead to increased blood volume: the following factors can lead to sodium retention: 1 glomerular filtration rate (GFR) decreased, sodium and sodium excretion decreased; 2 renin-angiotensin-aldosterone system activation, Aldosterone promotes sodium reabsorption in distal renal tubules and collecting ducts; 3 sympathetic nervous system activation promotes sodium reabsorption in proximal tubules; 4 decreases in nitric oxide (NO) production, decreases renal tubular sodium excretion; 5 renal function Incomplete insulin leads to increased insulin levels in the body. Stimulation of sodium pump (Na-K-ATPase) increases sodium reabsorption in the proximal tubules. Significant sodium retention can lead to volumetric hypertension.
(2) Increased vascular resistance: There are mechanisms that cause peripheral and renal arteries to contract, and increased vascular resistance: 1 activation of the renin-angiotensin-aldosterone system, activation of the sympathetic nervous system, and increased synthesis of endothelin, all of which stimulate vasoconstriction; 2NO production decreased, antagonism of vasoconstriction factors decreased; 3GFR decreased lead to increased parathyroid hormone secretion, extracellular volume expansion stimulated release of endogenous quetiapine, parathyroid hormone and quetiapine increased intracellular Ca2 concentration, promoted Vasoconstriction, and improve the sensitivity of the smooth muscle of the wall to vasoconstrictors; 4 insulin resistance, high insulin levels stimulate vascular smooth muscle hypertrophy, enhance vascular responsiveness, thickened wall, narrowing of lumen, increased vascular resistance, these factors Can lead to resistance hypertension.
In renal parenchymal hypertension, simple volumetric hypertension or simple resistance hypertension is rare, and most patients have two pathogenic factors, compared with essential hypertension, renal hypertension. Volume factors are often more pronounced.
It can be seen from the above that regardless of the occurrence of volumetric or resistance hypertension, many neurohumoral factors are involved, and Table 2 summarizes briefly.
Pathogenesis
The main mechanism of acute renal parenchymal disease leading to hypertension is sodium retention, increased blood volume, diuretic often lowers blood pressure, and even normal, while the pathogenesis of chronic renal parenchymal hypertension is complicated, which can be caused by many factors.
1. Factors that lead to high blood pressure
(1) Renin-angiotensin aldosterone system (RAAS) activation: There has been a large amount of data confirming that RAAS plays an important role in the development and progression of renal essential hypertension, and there is a lack of renal parenchymal disease. Blood can cause RAAS activation. Angiotensin II (AII) can directly stimulate vasoconstriction, increase sympathetic nerve activity through the central nervous system, and promote the release of catecholamines from sympathetic nerve endings, further promoting vasoconstriction; aldosterone can increase far The renal tubules and collecting tubes are reabsorbed by sodium, which aggravates sodium and water retention. Therefore, RAAS activation can participate in both resistance and volumetric hypertension.
(2) Sympathetic nerve excitability: The sympathetic nerve also plays an important role in the pathogenesis of renal parenchymal hypertension. In renal parenchymal disease, sympathetic nerves can be activated by afferent renal reflexes, and AII increase will also be from the center. And peripheral increases its activity, sympathetic nervous system activation can stimulate vasoconstriction, increase vascular resistance; can promote proximal renal tubular sodium reabsorption, increase blood volume, it can participate in hypertension and sympathetic nervous system activation from both resistance and volume It can also cause renal vasoconstriction and reduce renal blood flow and stimulate
Renin secretion further activates RAAS to increase weight.
(3) Endogenous digitalis-like substance release: can cross-react with digitalis antibody Endogenous digitalislike substance (EDIS) has the following characteristics: inhibition of Na-K-ATPase, promotion of sodium excretion, When the renal parenchymal disease causes the extracellular volume to expand, it can reflect and stimulate the release of EDIS from the hypothalamic brain tissue, inhibit Na-K-ATPase in the proximal renal tubular epithelial cells, reduce sodium reabsorption, and cause sodium excretion effect, however, On the other hand, EDIS will inhibit Na-K-ATPase in vascular smooth muscle, increase intracellular sodium concentration, reduce transmembrane sodium gradient, reduce Na/Ca2 exchange and voltage-dependent Ca2 channel depolarization, so intracellular Ca2 increases. This promotes the development of resistance hypertension.
(4) Endothelin: Endothelin is the most potent vasopressin found in the body, it may play a role through the endocrine pathway, as well as autocrine and paracrine pathways, endothelin can stimulate vasoconstriction; promote RAAS activation; reduce kidney Blood flow and GFR reduce urinary sodium excretion. Therefore, it may also participate in the pathogenesis of renal hypertension from both resistance and volume.
(5) arginine vasopressin: arginine vasopressin has little effect on blood pressure in normal and essential hypertension patients, but clinical trials have shown that arginine vasopressin is applied to patients with chronic renal failure. Antagonists can effectively reduce hypertension, suggesting that arginine vasopressin can participate in the development of hypertension in renal failure patients through vasoconstriction, but more research is needed to confirm this observation and clear mechanism of action.
(6) reduction of blood pressure lowering factor: the kidney can produce a variety of blood pressure lowering factors, such as prostaglandin E2 and I2, kinin (remote renal tubular epithelial cells produce kallikrein, which converts plasma kininogen to kinin ), atrial natriuretic peptide, brain natriuretic peptide, NO and medullary antihypertensive lipids, etc., as described above, N0 production is reduced in renal parenchymal disease, antagonism of vasoconstriction is weakened, and NO reduction can also reduce renal tubular sodium excretion, Aggravating sodium and water retention, it can participate in the pathogenesis of hypertension from both resistance and volume. However, it has not yet obtained conclusive evidence that other blood pressure lowering factors are involved in the onset of renal hypertension.
Prevention
Kidney substantial hypertension prevention
Prevention and active treatment of primary kidney disease is the key to prevention and treatment of renal hypertension.
Complication
Renal substantial hypertension complications Complications, renal failure, hypertensive encephalopathy
Can be complicated by complications such as renal failure and hypertensive encephalopathy.
Symptom
Renal substantial hypertension symptoms common symptoms refractory hypertension hyperuricemia pulse pressure micro-inflammation state glucose metabolism disorder hematuria hyperhomocysteinemia urinary protein metabolic acidosis renal interstitial fibrosis
Various symptoms of hypertension, renal hypertensive hypertension also exists, no longer repeat, only some specific aspects of renal manifestations of hypertension are described below.
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 is about twice that of the latter. Among them, IgA nephropathy, especially hyperplasia or sclerosing IgA nephropathy is particularly common in malignant hypertension, and the prognosis of renal malignant hypertension is worse than that of primary malignant hypertension. According to the authors, the former has a 5-year kidney survival rate of 60%, while the latter is one and a half years old. Kidney survival rate is only 4%.
Fundus lesions of renal parenchymal hypertension are often more severe, and heart 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 nephrotic syndrome. Lipid metabolism disorder, glucose metabolism disorder in diabetic nephropathy, anemia in renal insufficiency, hyperuricemia, hyperhomocysteinemia, uremic toxin, metabolic acidosis and microinflammation, etc. 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, and systemic hypertension is easily transmitted. Into the glomerulus, resulting in glomerular high pressure, high perfusion and high filtration, this "three high" can accelerate the residual glomerular sclerosis; at the same time, long-term high blood pressure can lead to small arteriosclerosis, including small balls Arterial glass-like changes, interlobular arteries and arcuate arterial intimal thickening, narrowing the lumen of the small arterial wall, secondary renal ischemia
Damage (glomerular ischemic contraction to ischemic sclerosis, tubular atrophy and renal interstitial fibrosis), so renal hypertension that is not well controlled will significantly accelerate the progression of renal parenchymal disease and form malignancy. cycle.
The glomerular disease with a large amount of urinary protein and the renal damage of hypertension are more obvious. Because of the superposition of the two effects, it is known that proteinuria, especially a large amount of proteinuria, can cause glomerular hypertension, high perfusion and high filtration. Promotes glomerular sclerosis; and, filtered proteins (including complement and growth factors, etc.) and certain substances that bind to proteins (including lipids and iron) are reabsorbed by the renal tubules to activate tubular cells and release Pathogenic factors (such as transforming growth factor beta) promote renal interstitial fibrosis, therefore, it is necessary to strictly control hypertension in patients with renal hypertension who have proteinuria.
Examine
Examination of renal parenchymal hypertension
According to the specific renal parenchymal lesions, laboratory tests have their own characteristics, such as acute glomerulonephritis: urinary hematuria, proteinuria with transient azotemia, chronic glomerulonephritis: a large amount of protein in the urine of patients, often There are red blood cells and casts, anemia and impaired renal function, chronic pyelonephritis: a history of urinary tract infection, traces of small or small amounts of protein in the urine, a small amount of red blood cells and white blood cells, positive urine culture.
1. B-ultrasound of the kidney showed diffuse lesions in both kidney parenchyma, thinning of the renal cortex, etc.; there were corresponding imaging changes in the primary disease.
2. The fundus may have retinal hemorrhage, exudation and optic disc edema.
Diagnosis
Diagnosis and diagnosis of renal parenchymal hypertension
diagnosis
The main diagnostic points of renal parenchymal hypertension are: patients are generally younger; there is a history of kidney disease; limbs are often wet and cold, pale; blood pressure is characterized by higher diastolic blood pressure, small pulse pressure, small blood pressure fluctuations; often kidney disease Signs such as anemia, hematuria, proteinuria, nocturia, renal function damage to varying degrees; B-ultrasound showed diffuse lesions in both kidney parenchyma, thinning of the renal cortex.
Differential 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. It is easily misdiagnosed as primary. hypertension.
1. Renal vascular hypertension is caused by various causes of unilateral or bilateral renal artery trunk or branch stenosis caused by hypertension, common causes are arteritis, fibromuscular dysplasia and atherosclerosis, such as with the following Clinical characteristics of hypertension should be suspected of this disease: occurred in patients under the age of 30 or over 50 years old, no family history of hypertension; hypertension has a short course, rapid progress, most of them show malignant hypertension; retina can have bleeding, seepage Out, optic disc edema, etc.; vocal murmur can be heard in the head and neck, upper abdomen and/or lower back ridge area; X-ray and B-ultrasound examination show the size and density of kidneys; renal venous blood test increases the renin activity of the affected side , captopril (captopril) radionuclide renal examination was positive, 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, or proteinuria first, plays a key role in differential diagnosis, The latter diagnosis points are as follows: 1 more common in middle age, may have a family history of hypertension; 2 more than 10 years of persistent hypertension before renal damage; 3 slow progression of the disease, renal tubular dysfunction (urinary concentrating function decline, There is an increase in nocturia) earlier than glomerular dysfunction; 4 mild urine changes (low urine protein, less urinary microscopy); 5 often associated with hypertensive retinopathy, heart, brain complications; 6 diagnosis of the disease still Need to exclude a variety of primary, secondary kidney disease, clinical diagnosis is indeed difficult when renal biopsy is feasible, renal tissue pathological examination is helpful for differential diagnosis.
3. Other secondary hypertension 1 Endocrine hypertension: hypercortisolism in endocrine disorders, pheochromocytoma, primary aldosteronism, hyperthyroidism and menopause can occur in high blood pressure, generally Can be based on endocrine history, special clinical manifestations and endocrine test to make a corresponding diagnosis, 2 aortic constriction, congenital aortic coarctation or multiple arteritis caused by descending aorta and abdominal aortic stenosis, can lead to hypertension 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 collateral circulation arteries. Pulsation, tremors and murmurs; signs of left ventricular hypertrophy and dilatation, 3 craniocerebral lesions: some encephalitis or tumors, intracranial hypertension, etc. often have hypertension, the neurological manifestations of this type of lesions are characteristic, the diagnosis is general Not difficult, 4 pregnancy-induced hypertension syndrome: more than 3 to 4 months after the third trimester of pregnancy, during childbirth or 48 hours after delivery, characterized by hypertension, edema and proteinuria The heavy ones have convulsions and coma.
