renal aspect of hypertension

Renal aspect of hypertension

How the kidney helps to maintain blood pressure?

The kidney functions as the long-term control mechanism for arterial pressure. This is largely linked to the ability of the kidney to maintain balance between fluid intake and output in the body. Among the functions of kidney:
1. Maintain normal sodium balance
2. Maintain ECF volume
3. Maintain normal blood volume at normotensive arterial pressures.

Chronic hypertension:

Caused by impaired renal function (unable to excrete fluid efficiently)
1. Volume-loading hypertension:
When a person with impaired kidney consumes a lot of water and salt, this will increase the ECF volume, increase the blood volume, and eventually CO. However, the baroreceptor reflex mechanism will act to decrease TPR of the vascular to maintain the normal MAP. After few days, the barorecepter adapt(reset), and the TPR begin to increase as the “autoregulation” mechanism constricts all the vascular to maintain normal blood flow. This leads to increase in MAP.

2. Hypertension due to primary aldosteronism:
Tumor in one of the adrenal glands causes the glands to secrete excess aldosterone hormones, leading to ‘primary aldosteronism’. Aldosterone act to increase salt and water reabsorption by the tubules of the kidneys. Less urine will be excreted and the ECF volume will increase as well as the blood volume. Eventually, this will lead to hypertension.

Hypertension involving renin-angiotensin system:
1. “One-kidney” Goldblatt hypertension:
One kidney is removed and the renal artery is constricted, the pressure in the renal artery will decreased, causing kidney to release renin enzyme. Renin will then produce angiotensin I and II which have direct effect to constrict blood vessels and longer term effect of retaining salt and water in kidney. This in turn will increase the MAP.

2. “Two-kidney Goldblatt hypertension:
Artery to one of the kidney is constricted while the other is normal. The constricted kidney secrete renin, produce angiotensin which affects both kidney. The same processes occur and hypertension develops.

3. Hypertension by diseased kidney:
Constriction or haemorrhage in one kidney decreases the blood flow in renal artery. Kidney will release renin and the same event as in two-kidney hypertension occurs.

Other types of hypertension:
1. Hypertension in upper part of body caused by coarctation of aorta.
2. Hypertension in preeclampsia (toxaemia of pregnancy).
3. Neurogenic hypertension.

Primary(essential) hypertension:Unknown origin of hypertension. Most of ptx appears to have sedentary lifestyle and overweight. This leads to:
1. Increased CO:
a. Additional blood flow required for extra adipose tissue.
b. Increased blood flow in heart, kidneys, GI tract, skeletal muscle due to increased metabolic rate and organ growth in respond to increased metabolic demands.
c. Consequently, increased TPR.

2. Increased sympathetic nerve activity:
a. Leptin hormone is released from fat cells and stimulate multiple regions on hypothalamus, leads to excitatory influence on vasomotor centers of medulla.

3. Angiotensing II and aldosterone levels increased 2,3 fold in obese ptx:
a. Increased sympathetic nerve activity.

4. Impaired renal-pressure natriuresis mechanism:
a. Kidney excrete less salt and water unless there’s high arterial pressure.

Investigations for hypertension due to kidney failure:

Urine test:
1. Appearance: bloody, dark, smoky, plain.

2. Volume: Lower in ptx with hypertension.

3. Chemical (stix) testing: test the urine for blood, protein and sugar.
a. Blood: haematuria. highly sensitive. Can be positive even there’s only 1 or 2 red cells.
b. Protein: proteinuria. The stix react with albumin and insensitive to globulin. High protein indicates kidney failure.
c. Microalbuminuria: albumin leak into urine since kidney fail to separate from it from wastes.

Calculation of protein-to-creatinine ratio. Creatinine is waste product in blood produced during normal breakdown of muscle cells during activity. Impaired kidney will cause builds up of creatinine in blood.

Glomerular filtration rate (GFR):
1. To calculate how efficient the kidney filter waste from blood. It requires withdrawal of blood and testing for creatinine levels.

Blood urea nitrogen:
1. Blood carries protein to cells throughout the body. After the cells use the protein, the remaining waste product is returned to the blood as urea, a compound containing nitrogen. If a person’s kidneys are not working well, the urea will stay in the blood.

2. A deciliter of normal blood contains 7 to 20 milligrams of urea. If a person’s BUN is more than 20 mg/dL, the kidneys may not be working at full strength. Other possible causes of an elevated BUN include dehydration and heart failure.

other techniques:
1. Radionucleotide studies: can demonstrate decreased renal perfusion on affected side. Disproportionate fall in uptake of substance on affected side following administration ofACE inhibitor or NSAIDs suggest presence of significant renal artery stenosis.
2. Doppler ultrasound: generates data about intrarenal vascular resistance.
3. MRA: magnetic resonance angiography. Visualize renal arteries to see comparison with findings of renal arteriography.
4. Renal arteriography: use a contrast medium to inject into artery via a fine transfemoral arterial catheter (arterial digital subtraction angiography). Used to define extrarenal or intrarenal arterial disease.