Renal Parenchymal Hypertension

Chapter: Renal Parenchymal Hypertension
McMaster Section Editor(s): Christine M. Ribic, Karen C.Y. To
Section Editor(s) in Interna Szczeklika: Franciszek Kokot, Robert Drabczyk
McMaster Author(s): K. Scott Brimble
Author(s) in Interna Szczeklika: Andrzej Więcek, Jerzy Chudek
Additional Information

Definition, Etiology, PathogenesisTop

Renal parenchymal hypertension is a form of secondary hypertension caused by kidney disease. It may occur in the course of glomerulonephritis, diabetic nephropathy (diabetic kidney disease), kidney damage in the course of systemic connective tissue diseases (systemic lupus erythematosus, systemic sclerosis, systemic vasculitis), tubulointerstitial nephritis, obstructive nephropathy, polycystic kidney disease, large solitary kidney cysts (rare), postirradiation nephropathy, hypoplastic kidney, renal tuberculosis (rare).

The main mechanisms leading to hypertension in chronic kidney disease (CKD) include impaired urinary sodium and water excretion (impaired pressure natriuresis); excessive kidney release of vasoconstrictors (angiotensin II and endothelin 1); vasodilator deficiency (eg, NO); sympathetic activation; endocrine and metabolic disturbances (including calcium/phosphate metabolism). The accelerated development of atherosclerosis and calcification of the vascular wall leads to an increased stiffness of the walls of large arteries. Sodium and water retention with subsequent volume overload increase with progression of kidney disease. An increase in venous return and cardiac output causes sympathetic activation, which results in increased vasoconstriction of the resistance vessels and an increase in peripheral vascular resistance.

Clinical Features and Natural HistoryTop

Hypertension often develops at an early stage of kidney disease, when the glomerular filtration rate (GFR) is only slightly reduced (it may be the presenting feature). Symptoms of the underlying kidney disease are usually the predominant clinical feature. Sodium and water retention manifest as peripheral edemas only in some patients. Untreated hypertension accelerates the progression of kidney disease and may itself be a cause of (hypertensive) nephropathy. Kidney diseases are the most common causes of treatment-resistant and malignant hypertension.

DiagnosisTop

Perform the same diagnostic tests as in all patients with hypertension (see Essential Hypertension) as well as studies necessary for the diagnosis of the kidney disease responsible for the hypertension. Note that there may be other contributors to hypertension in patients with renal parenchymal disease, including renovascular disease and drug therapy (erythropoietin-stimulating agents, calcineurin inhibitors). Consider also unrecognized nonsteroidal anti-inflammatory drug (NSAID) use as a potential contributor to both hypertension and CKD.

TreatmentTop

General Considerations

1. Treatment of renal parenchymal hypertension involves treating the underlying kidney disease and hypertension.

2. Target blood pressure: <140/90 mm Hg in all patients (exceptions: see Essential Hypertension); according to the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (NKF KDOQI) guidelines, the target blood pressure levels are ≤130/80 mm Hg in patients with proteinuria >1 g/d and in patients after kidney transplantation, and <140/90 mm Hg in patients treated with renal replacement therapy (RRT). For general principles, see Essential Hypertension.

Nonpharmacologic Management

1. Restriction of salt intake (sodium chloride) to 5 to 6 g/d.

2. Monitoring fluid balance to maintain normal volume status (this is of particular importance in patients on dialysis).

Pharmacotherapy

1. Drug selection: Angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) are preferred in patients with CKD and proteinuria, but these two classes should not be used in combination. As in other patients treated with these agents, the risk of acute kidney injury is increased with dehydration, generalized atherosclerosis, and heart failure.

Diuretics are a key component of blood pressure control in patients with renal parenchymal disease. Use thiazide diuretics in patients with a GFR ≥30 mL/min/1.73 m2 and loop diuretics in patients with a GFR <30 mL/min/1.73 m2 and/or with severe proteinuria and edema. Potassium-sparing diuretics should be used cautiously, if at all, due to the risk of hyperkalemia. Further agents that can be used include calcium channel blockers and cardioselective beta-blockers. Other agents, including alpha-blockers, centrally acting alpha-agonists, or vasodilators, are typically reserved for adjunctive therapy when alternative drugs are insufficient to control blood pressure and/or are not tolerated. With advancing CKD, attention to the route of excretion of the various agents should be reviewed.

Starting treatment with an ACEI or ARB:

1) In patients who have not been previously treated with antihypertensive agents, start with an intermediate dose of an ACEI or ARB and titrate it up every 4 to 8 weeks, checking the serum estimated glomerular filtration rate (eGFR) and potassium levels prior to the initiation and 2 to 4 weeks following the initiation or dose escalation.

2) In patients who are already treated with antihypertensive drugs, add an ACEI or ARB at a low dose and titrate it up while reducing the dose of the previously used antihypertensive agent(s) at the same time.

2. Monitoring of treatment with ACEIs/ARBs: In patients with a reduced GFR in whom treatment with an ACEI or ARB has been started or the dose of the agent has been increased, monitor the following parameters at time intervals dependent on their baseline values (Table. Monitoring of serum creatinine (GFR)…):

1) eGFR: In patients with a substantial decrease in the GFR (eg, >10%), closer monitoring is recommended, as this is associated with an increased risk of adverse cardiovascular and renal events and our practice is not to escalate the doses of the ACEI/ARB in such situations. In patients with a GFR decrease >30% from baseline, consider a dose reduction or switch to an antihypertensive agent from another class. In patients who are on a diuretic and may be volume depleted, consider reducing the diuretic dose and rechallenging with the ACEI/ARB at a reduced dose.

2) Serum potassium levels:

a) 5.1 to 5.5 mmol/L: Recommend restricted consumption of potassium-rich foods (renalnetwork.on.ca) and reduce the doses or discontinue other drugs that may increase potassium levels if the potassium level does not fall into an acceptable range.

b) 5.6 to 5.9 mmol/L: Recommend restricted consumption of potassium-rich foods, reduce the dose of the ACEI/ARB by 50% or add a diuretic, and measure serum potassium levels approximately every week until they return to an acceptable range. If this does not occur within 4 weeks, either discontinue the ACEI/ARB and use an antihypertensive drug from another class, or consider potassium-binding therapy (eg, Kayexalate).

c) >5.9 mmol/L: Consider the need for a more urgent evaluation, discontinue the ACEI/ARB, recommend restricted consumption of potassium-rich foods, and reduce the doses or discontinue other drugs that may increase potassium levels. Consider reinitiation of the ACEI/ARB at a reduced dose if the serum potassium level normalizes.

After establishing dose(s) of the drug(s) and achieving stable blood pressure, GFR, and potassium levels, serum creatinine and potassium levels are monitored less frequently (Table. Monitoring of serum creatinine (GFR)…).

In patients with an eGFR falling to <15 mL/min/1.73 m2, discontinuation of ACEIs/ARBs in some cases may improve the GFR and delay the need to start RRT.

TablesTop

Table. Monitoring of serum creatinine (GFR) and serum potassium levels during treatment with an ACEI or ARB in patients with chronic kidney disease

GFR (mL/min/1.73 m2)

Serum potassium level (mmol/L)

After treatment initiation or dose change

In a stable patienta,b

≥60

≤4.5

In 2-4 weeks

Every 6-12 months

30-59

4.6-5

In 2-4 weeks

Every 3-6 months

<30

5.1-5.5

In 2 weeks

Every 2-4 months

a After determining dosage and stabilizing blood pressure, GFR, and serum potassium level.

b In patients with a decrease in the GFR ≥15% during ACEI or ARB treatment, measure serum creatinine levels (GFR) every 1 to 2 months.

ACEI, angiotensin-converting enzyme inhibitor; ARB, angiotensin receptor blocker; GFR, glomerular filtration rate.

 

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