Hypertensive kidney disease

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Hypertensive kidney disease
Other namesHypertensive nephrosclerosis (HN or HNS), hypertensive kidney disease, hypertensive nephropathy (HN), nephroangiosclerosis [1]
Renal arterial hyalinosis - pas - very high mag.jpg
Micrograph showing renal arterial hyalinosis – pink ring right-of-centre. PAS stain.
Specialty Nephrology   OOjs UI icon edit-ltr-progressive.svg

Hypertensive kidney disease is a medical condition referring to damage to the kidney due to chronic high blood pressure. It manifests as hypertensive nephrosclerosis (sclerosis referring to the stiffening of renal components). [2] It should be distinguished from renovascular hypertension, which is a form of secondary hypertension, and thus has opposite direction of causation.

Contents

Signs and symptoms

Signs and symptoms of chronic kidney disease, including loss of appetite, nausea, vomiting, itching, sleepiness or confusion, weight loss, and an unpleasant taste in the mouth, may develop. [3]

Causes

On gross pathology, nephrosclerosis manifests as a fine granular surface. Gross pathology of nephrosclerosis.jpg
On gross pathology, nephrosclerosis manifests as a fine granular surface.

"Hypertensive" refers to high blood pressure and "nephropathy" means damage to the kidney; hence this condition is where chronic high blood pressure causes damages to kidney tissue; this includes the small blood vessels, glomeruli, kidney tubules and interstitial tissues. The tissue hardens and thickens which is known as nephrosclerosis. [2] The narrowing of the blood vessels means less blood is going to the tissue and so less oxygen is reaching the tissue resulting in tissue death (ischemia). [5]

Risk factors for HN include poorly controlled, moderate-to-severe hypertension, older age, other kidney disorders, and Afro-Caribbean background, whose exact cause is unclear, as it may be due to either genetic susceptibility or poor health management among people of Afro-Caribbean descent. [2]

Mechanism

In the kidneys, as a result of benign arterial hypertension , hyaline (pink, amorphous, homogeneous material) accumulates in the walls of small arteries and arterioles, producing the thickening of their walls and the narrowing of the arterial openings, a process known as arteriolosclerosis. The resulting inadequate blood flow produces tubular atrophy, interstitial fibrosis, and glomerular alterations (smaller glomeruli with different degrees of hyalinization – from mild to sclerosis of glomeruli) and scarring around the glomeruli (periglomerular fibrosis). In advanced stages, kidney failure will occur. Functional nephrons [6] have dilated tubules, often with hyaline casts in the opening of the tubules. Additional complications often associated with hypertensive nephropathy include glomerular damage resulting in protein and blood in the urine.[ citation needed ]

Hypertensive nephropathy refers to kidney failure that can be attributed to a history of hypertension [7] It is a chronic condition and it is a serious risk factor for the development of end-stage kidney disease (ESKD). However, despite the well-known association between hypertension and chronic kidney disease, the underlying mechanism remains unclear. The two proposed mechanisms of HN's pathophysiology [8] both centre around how the glomerulus, a network of dense capillaries that carries out the kidney filtration process, is affected; with one theory identifying glomerular ischemia as the main contributor to HN and the other identifying glomerular hypertension and glomerular hyperfiltration at the centre of HN's pathogenesis. [7]

Glomerular ischemia

High blood pressure in the long term can damage the endothelium, commonly known as the blood vessel lining. This leads to a build-up of plaques and they can be deposited in the renal arteries causing stenosis and ischemic kidney disease.[ citation needed ] In this situation, the kidney supplied blood by the narrowed renal artery suffers from inadequate blood flow, which in turn causes the size of the kidneys to decrease. Other consequences include arterial stiffening, which involves a gradual breakdown of elastic fibers and intima (the innermost layer of a blood vessel) thickening.[ citation needed ]

Glomerular hypertension and glomerular hyperfiltration

An alternative mechanism of hypertensive nephropathy is prolonged glomerular hypertension and hence glomerular hyperfiltration. These can occur simultaneously but not necessarily. The idea is that hypertension results in sclerosis of the glomeruli which ultimately means reduced kidney function. As a compensatory mechanism, the unaffected nephrons (specifically, the preglomerular arterioles) vasodilate to increase blood flow to the kidney perfusion and increase glomerular filtration across undamaged glomeruli.[ citation needed ]

Diagnosis

Diagnosis of HN is made from clinical history and biochemical investigations. Chronic hypertension with progressive kidney disease progresses over a long period of time. Damage to the glomeruli allows proteins that are usually too large to pass into the nephron to be filtered. This leads to an elevated concentration of albumin in the urine (albuminuria). This albuminuria usually does not cause symptoms but can be indicative of many kidney disorders. Protein in the urine (proteinuria) is best identified from a 24-hour urine collection. [9]

Bilateral renal artery stenosis should always be considered as a differential diagnosis for the presentation of HN. Kidney disease with this etiology can potentially be reversed following vascular intervention.[ citation needed ]

Histology

In benign nephrosclerosis, the changes occurring are gradual and progressive, however, there can be sufficient kidney reserve capacity to maintain adequate kidney function for many years. [10] The large renal arteries exhibit intimal thickening, medial hypertrophy, duplication of the elastic layer. The changes in small arterioles include hyaline arteriolosclerosis (deposition of hyaline, collagenous material),[ citation needed ] which causes glomerular collapse (wrinkling and thickening of capillary basement membranes and collapse of capillary lumen) and solidification (glomeruli exhibit sclerosis and increase in mesangial matrix). The degree of scarring correlates with the degree of glomerular filtration deficit.[ citation needed ]

Malignant nephrosclerosis is where hypertensive nephrosclerosis occurs in presence of malignant hypertension (when DBP > 130mmHg). [11] Vessels feature intimal thickening, fibrinoid necrosis, red blood cell fragmentation, extravasation, thrombosis. These changes create an exaggerated layered appearance (onion skinning). [12]

Urine test

Microalbuminuria (moderate increase in the levels of urinary albumin) is a non-specific finding in patients with vascular disease that is associated with increased risk of cardiovascular events. The majority of patients with benign nephrosclerosis have proteinuria in the range from 0.5 to 1 g/ 24hr. In the case of glomerular damage occurring in HN, hematuria can occur as well.[ citation needed ]

Definitive diagnosis

The definitive diagnosis of HN requires morphological examination. Common histological features can be identified in the renal and glomerular vasculature. Glomerulosclerosis is often present, either focally or globally, which is characterized by hardening of the vessel walls. Also, luminal narrowing of the arteries and arterioles of the kidney system. However, this type of procedure is likely to be preceded by a provisional diagnosis based on laboratory investigations.[ citation needed ]

Future diagnostic approaches

Increasing access to, and use of, genome profiling may provide opportunity for diagnosis based on presentation and genetic risk factors, by identifying ApoL1 gene variants on chromosome 22. [13]

Management

The aim of the medical treatment is to slow the progression of chronic kidney disease by reducing blood pressure and albumin levels. [14] The current published guidelines define ideal BP of <130/80 mmHg for patients with hypertensive nephropathy; studies show that anything higher or lower than this can increase cardiovascular risk. According to the African American Study of Kidney Disease (AASK) trial, after an additional 5 years follow-up upon completion of the 10-year trial, up to 65% of the cohort had progressive nephropathy despite having controlled the mean systolic BP level <135 mmHg. [15]

ACE inhibitors, angiotensin receptor blockers, direct renin inhibitors and aldosterone antagonists, are pharmacological treatments that can be used to lower BP to target levels; hence reducing neuropathy and proteinuria progression. The management plan should be individualized based on the condition of the patients including comorbidities and previous medical history. [16] In addition, there are lifestyle changes that can be made. Weight reduction, exercise, reducing salt intake can be done to manage hypertensive nephropathy.[ citation needed ]

Prognosis

According to the United States Renal Data System (USRDS), hypertensive nephropathy accounts for more than one-third of patients on hemodialysis and the annual mortality rate for patients on hemodialysis is 23.3%. Haemodialysis is recommended for patients who progress to end-stage kidney disease (ESKD) and hypertensive nephropathy is the second most common cause of ESKD after diabetes. Patient prognosis is dependent on numerous factors including age, ethnicity, blood pressure and glomerular filtration rate. Changes in lifestyle factors, such as reduced salt intake and increased physical activity have been shown to improve outcomes but are insufficient without pharmacological treatment.[ citation needed ]

Epidemiology

The incidence of hypertensive nephropathy varies around the world. For instance, it accounts for as many as 25% and 17% of patients starting dialysis for end-stage kidney disease in Italy and France respectively. Contrastingly, Japan and China report only 6 and 7% respectively. Since the year 2000, nephropathy caused by hypertension has increased in incidence by 8.7% [17] In reality, these figures may be even higher, as hypertension is not always reported as the specific cause of kidney disease. [18]

It has been recognized that the incidence of hypertensive nephropathy varies with ethnicity. Compared to Caucasians, African Americans in the USA are much more likely to develop hypertensive nephropathy. [19] Of those who do, the proportion who then go on to develop end-stage kidney failure is 3.5 times higher than in the Caucasian population. In addition to this, African Americans tend to develop hypertensive nephropathy at a younger age than Caucasians (45 to 65, compared to >65). [7]

See also

Related Research Articles

<span class="mw-page-title-main">Kidney</span> Organ that filters blood and produces urine

In humans, the kidneys are two reddish-brown bean-shaped blood-filtering organs that are a multilobar, multipapillary form of mammalian kidneys, usually without signs of external lobulation. They are located on the left and right in the retroperitoneal space, and in adult humans are about 12 centimetres in length. They receive blood from the paired renal arteries; blood exits into the paired renal veins. Each kidney is attached to a ureter, a tube that carries excreted urine to the bladder.

<span class="mw-page-title-main">Proteinuria</span> Presence of an excess of serum proteins in the urine

Proteinuria is the presence of excess proteins in the urine. In healthy persons, urine contains very little protein, less than 150 mg/day; an excess is suggestive of illness. Excess protein in the urine often causes the urine to become foamy. Severe proteinuria can cause nephrotic syndrome in which there is worsening swelling of the body.

<span class="mw-page-title-main">Nephron</span> Microscopic structural and functional unit of the kidney

The nephron is the minute or microscopic structural and functional unit of the kidney. It is composed of a renal corpuscle and a renal tubule. The renal corpuscle consists of a tuft of capillaries called a glomerulus and a cup-shaped structure called Bowman's capsule. The renal tubule extends from the capsule. The capsule and tubule are connected and are composed of epithelial cells with a lumen. A healthy adult has 1 to 1.5 million nephrons in each kidney. Blood is filtered as it passes through three layers: the endothelial cells of the capillary wall, its basement membrane, and between the foot processes of the podocytes of the lining of the capsule. The tubule has adjacent peritubular capillaries that run between the descending and ascending portions of the tubule. As the fluid from the capsule flows down into the tubule, it is processed by the epithelial cells lining the tubule: water is reabsorbed and substances are exchanged ; first with the interstitial fluid outside the tubules, and then into the plasma in the adjacent peritubular capillaries through the endothelial cells lining that capillary. This process regulates the volume of body fluid as well as levels of many body substances. At the end of the tubule, the remaining fluid—urine—exits: it is composed of water, metabolic waste, and toxins.

<span class="mw-page-title-main">Nephritis</span> Inflammation of the kidneys

Nephritis is inflammation of the kidneys and may involve the glomeruli, tubules, or interstitial tissue surrounding the glomeruli and tubules. It is one of several different types of nephropathy.

<span class="mw-page-title-main">Juxtaglomerular apparatus</span> Structure that regulates function of each nephron

The juxtaglomerular apparatus is a structure in the kidney that regulates the function of each nephron, the functional units of the kidney. The juxtaglomerular apparatus is named because it is next to (juxta-) the glomerulus.

<span class="mw-page-title-main">Assessment of kidney function</span> Ways of assessing the function of the kidneys

Assessment of kidney function occurs in different ways, using the presence of symptoms and signs, as well as measurements using urine tests, blood tests, and medical imaging.

<span class="mw-page-title-main">Glomerulus (kidney)</span> Functional unit of nephron

The glomerulus is a network of small blood vessels (capillaries) known as a tuft, located at the beginning of a nephron in the kidney. Each of the two kidneys contains about one million nephrons. The tuft is structurally supported by the mesangium, composed of intraglomerular mesangial cells. The blood is filtered across the capillary walls of this tuft through the glomerular filtration barrier, which yields its filtrate of water and soluble substances to a cup-like sac known as Bowman's capsule. The filtrate then enters the renal tubule of the nephron.

<span class="mw-page-title-main">Chronic kidney disease</span> Medical condition

Chronic kidney disease (CKD) is a type of kidney disease in which a gradual loss of kidney function occurs over a period of months to years. Initially generally no symptoms are seen, but later symptoms may include leg swelling, feeling tired, vomiting, loss of appetite, and confusion. Complications can relate to hormonal dysfunction of the kidneys and include high blood pressure, bone disease, and anemia. Additionally CKD patients have markedly increased cardiovascular complications with increased risks of death and hospitalization.

<span class="mw-page-title-main">IgA nephropathy</span> Disease of the kidney

IgA nephropathy (IgAN), also known as Berger's disease, or synpharyngitic glomerulonephritis, is a disease of the kidney and the immune system; specifically it is a form of glomerulonephritis or an inflammation of the glomeruli of the kidney. Aggressive Berger's disease can attack other major organs, such as the liver, skin and heart.

<span class="mw-page-title-main">Glomerulonephritis</span> Term for several kidney diseases

Glomerulonephritis (GN) is a term used to refer to several kidney diseases. Many of the diseases are characterised by inflammation either of the glomeruli or of the small blood vessels in the kidneys, hence the name, but not all diseases necessarily have an inflammatory component.

<span class="mw-page-title-main">Renal artery stenosis</span> Medical condition

Renal artery stenosis (RAS) is the narrowing of one or both of the renal arteries, most often caused by atherosclerosis or fibromuscular dysplasia. This narrowing of the renal artery can impede blood flow to the target kidney, resulting in renovascular hypertension – a secondary type of high blood pressure. Possible complications of renal artery stenosis are chronic kidney disease and coronary artery disease.

<span class="mw-page-title-main">Diabetic nephropathy</span> Chronic loss of kidney function

Diabetic nephropathy, also known as diabetic kidney disease, is the chronic loss of kidney function occurring in those with diabetes mellitus. Diabetic nephropathy is the leading causes of chronic kidney disease (CKD) and end-stage renal disease (ESRD) globally. The triad of protein leaking into the urine, rising blood pressure with hypertension and then falling renal function is common to many forms of CKD. Protein loss in the urine due to damage of the glomeruli may become massive, and cause a low serum albumin with resulting generalized body swelling (edema) so called nephrotic syndrome. Likewise, the estimated glomerular filtration rate (eGFR) may progressively fall from a normal of over 90 ml/min/1.73m2 to less than 15, at which point the patient is said to have end-stage renal disease. It usually is slowly progressive over years.

<span class="mw-page-title-main">Focal segmental glomerulosclerosis</span> Kidney disease

Focal segmental glomerulosclerosis (FSGS) is a histopathologic finding of scarring (sclerosis) of glomeruli and damage to renal podocytes. This process damages the filtration function of the kidney, resulting in protein presence in the urine due to protein loss. FSGS is a leading cause of excess protein loss—nephrotic syndrome—in children and adults. Signs and symptoms include proteinuria and edema. Kidney failure is a common long-term complication of the disease. FSGS can be classified as primary, secondary, or genetic, depending on whether a particular toxic or pathologic stressor or genetic predisposition can be identified as the cause. Diagnosis is established by renal biopsy, and treatment consists of glucocorticoids and other immune-modulatory drugs. Response to therapy is variable, with a significant portion of patients progressing to end-stage kidney failure. An American epidemiological study 20 years ago demonstrated that FSGS is estimated to occur in 7 persons per million, with males and African-Americans at higher risk.

<span class="mw-page-title-main">Arteriolosclerosis</span> Medical condition

Arteriolosclerosis is a form of cardiovascular disease involving hardening and loss of elasticity of arterioles or small arteries and is most often associated with hypertension and diabetes mellitus. Types include hyaline arteriolosclerosis and hyperplastic arteriolosclerosis, both involved with vessel wall thickening and luminal narrowing that may cause downstream ischemic injury. The following two terms whilst similar, are distinct in both spelling and meaning and may easily be confused with arteriolosclerosis.

<span class="mw-page-title-main">Renovascular hypertension</span> Medical condition

Renovascular hypertension is a condition in which high blood pressure is caused by the kidneys' hormonal response to narrowing of the arteries supplying the kidneys. When functioning properly this hormonal axis regulates blood pressure. Due to low local blood flow, the kidneys mistakenly increase blood pressure of the entire circulatory system. It is a form of secondary hypertension - a form of hypertension whose cause is identifiable.

<span class="mw-page-title-main">Loin pain hematuria syndrome</span> Medical condition

Loin pain hematuria syndrome (LPHS) is the combination of debilitating unilateral or bilateral flank pain and microscopic or macroscopic amounts of blood in the urine that is otherwise unexplained.

<span class="mw-page-title-main">Benign nephrosclerosis</span>

Benign nephrosclerosis refers to the renal changes most commonly occurring in association with long-standing hypertension. It is termed benign because it rarely progresses to clinically significant chronic kidney disease or kidney failure.

Diffuse proliferative glomerulonephritis (DPGN) is a type of glomerulonephritis that is the most serious form of renal lesions in SLE and is also the most common, occurring in 35% to 60% of patients. In absence of SLE, DPGN pathology looks more like Membranoproliferative glomerulonephritis

Sickle cell nephropathy is a type of nephropathy associated with sickle cell disease which causes kidney complications as a result of sickling of red blood cells in the small blood vessels. The hypertonic and relatively hypoxic environment of the renal medulla, coupled with the slow blood flow in the vasa recta, favors sickling of red blood cells, with resultant local infarction. Functional tubule defects in patients with sickle cell disease are likely the result of partial ischemic injury to the renal tubules.

<span class="mw-page-title-main">Complications of hypertension</span>

Complications of hypertension are clinical outcomes that result from persistent elevation of blood pressure. Hypertension is a risk factor for all clinical manifestations of atherosclerosis since it is a risk factor for atherosclerosis itself. It is an independent predisposing factor for heart failure, coronary artery disease, stroke, kidney disease, and peripheral arterial disease. It is the most important risk factor for cardiovascular morbidity and mortality, in industrialized countries.

References

  1. ↑ Fervenza, Fernando C (2016-09-08). Batuman, Vecihi (ed.). "Nephrosclerosis: Background, Pathophysiology, Epidemiology".
  2. 1 2 3 Zhang, Zhiwei. "Benign Hypertensive Arteriolar Nephrosclerosis". Merck Manuals Consumer Version. Retrieved 2016-11-12.
  3. ↑ "Benign Hypertensive Arteriolar Nephrosclerosis". MSD Manual Consumer Version. Retrieved 2016-11-12.
  4. ↑ Guenevere Rae, Ph.D., William Newman, M.D., Supriya Donthamsetty, M.D., Robin McGoey, M.D. "The Cadaver's Kidney P.G." (PDF). Retrieved 2021-05-18.{{cite web}}: CS1 maint: multiple names: authors list (link)
  5. ↑ "Hypertensive Nephropathy, Symptoms, Treatment, Diet and Causes – Kidney Disease Symptoms and Treatment". www.kidney-symptom.com. Archived from the original on 2019-06-07. Retrieved 2016-11-12.
  6. ↑ "nephron: definition of nephron in Oxford dictionary (American English) (US)". www.oxforddictionaries.com. Archived from the original on April 27, 2016. Retrieved 2016-04-15.
  7. 1 2 3 "Nephrosclerosis: Background, Pathophysiology, Epidemiology". 2016-09-08.
  8. ↑ Suneel Udani; Ivana Lazich; George L. Bakris. "Epidemiology of Hypertensive Kidney Disease".
  9. ↑ Rowe, D J; Bagga, H; Betts, P B (1985-09-14). "Normal variations in rate of albumin excretion and albumin to creatinine ratios in overnight and daytime urine collections in non-diabetic children". British Medical Journal (Clinical Research Ed.). 291 (6497): 693–694. doi:10.1136/bmj.291.6497.693. ISSN   0267-0623. PMC   1416648 . PMID   3929903.
  10. ↑ MD, Edward C. Klatt. "Renal Pathology". library.med.utah.edu. Retrieved 2016-11-12.
  11. ↑ "Malignant nephrosclerosis". Farlex medical dictionary, citing McGraw-Hill Concise Dictionary of Modern Medicine.
  12. ↑ "Renal Pathology".
  13. ↑ Parsa, Afshin; Kao, W. H. Linda; Xie, Dawei; Astor, Brad C.; Li, Man; Hsu, Chi-yuan; Feldman, Harold I.; Parekh, Rulan S.; Kusek, John W. (2013-12-05). "APOL1 risk variants, race, and progression of chronic kidney disease". The New England Journal of Medicine. 369 (23): 2183–2196. doi:10.1056/NEJMoa1310345. ISSN   1533-4406. PMC   3969022 . PMID   24206458.
  14. ↑ "Clinical features, diagnosis, and treatment of hypertensive nephrosclerosis". www.uptodate.com. Retrieved 2016-11-12.
  15. ↑ Hart, Peter D.; Bakris, George L. (2010-11-01). "Hypertensive nephropathy: prevention and treatment recommendations". Expert Opinion on Pharmacotherapy. 11 (16): 2675–2686. doi:10.1517/14656566.2010.485612. ISSN   1744-7666. PMID   20718588. S2CID   21605880.
  16. ↑ "Hypertension". The Lecturio Medical Concept Library. Retrieved 25 July 2021.
  17. ↑ Fervenza, Fernando (2015-03-30). "Nephrosclerosis". Medscape. Retrieved 2016-11-12.
  18. ↑ Yarnell, John; O'Reilly, Dermot (2013-05-23). Epidemiology and Disease Prevention: A Global Approach. OUP Oxford. ISBN   978-0-19-966053-7.
  19. ↑ Fogo, Agnes B. (2003-02-01). "Hypertensive risk factors in kidney disease in African Americans". Kidney International. Renal Disease in Racial and Ethnic Minority Groups. 63, Supplement 83 (83): S17–S21. doi: 10.1046/j.1523-1755.63.s83.5.x . PMID   12864869.

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