Australian Doctor 8th Nov Issue | Page 26

26 HOW TO TREAT : HIGH BLOOD PRESSURE AND CHRONIC KIDNEY DISEASE

26 HOW TO TREAT : HIGH BLOOD PRESSURE AND CHRONIC KIDNEY DISEASE

8 NOVEMBER 2024 ausdoc . com . au
pressure increases in parallel with
worsening stage of CKD ( ie , the lower the eGFR or the greater the albuminu-
Figure 1 . 3D illustration of the structure of a nephron .
The eGFR is automatically estimated from serum creatinine levels , patient age and gender , using a mathe-
ria and blood pressure , the higher the association with a subsequent risk of kidney failure ). 9 , 10 It has been estimated that up to 90 % of those
matical formula . An eGFR of less than 60mL / min / 1.73m 2 denotes abnormal kidney function , as it approximates an eGFR of more than two standard
with CKD have high blood pressure . 9 Equally , in studies of patients with
deviations below the mean eGFR of healthy individuals ( ie , it is out of the
high blood pressure , at least one in
normal range or ‘ abnormal ’, see fig-
three are reported to have CKD .
ure 5 ). The formula used to calculate
As a diagnosis of ‘ hypertensive
the eGFR is not perfect and serum
kidney disease ’ is one of exclusion ,
creatinine is variable on a day-to-day
its reported prevalence is highly var-
basis because of changes in hydration ,
iable and mostly determined by the
physical activity and diet . However , it
adequacy of the resources available to exclude other causes . 4 Some have argued that many of these patients actually have other ( undiagnosed )
will identify most patients who persistently have an eGFR of less than 60mL / min / 1.73m 2 ( ie , those most at risk of adverse kidney outcomes ).
forms of kidney disease , and mild to
Unless significantly ( greater than
moderate high blood pressure is not
20 %) less than previous values for any
the cause of their kidney disease , but rather is the result of it . 11 Indeed , the prevalence of reported hypertensive
individual , any eGFR found to be in the normal range can be followed with repeat screening at least annually , or
CKD does not correlate with that of
more often in individuals at increased
high blood pressure in the same popu-
risk of CKD ( eg , people with CVD ,
lations , but instead is associated with
high blood pressure or eGFR values
the prevalence of non-diabetic CKD . 4 Nonetheless , high blood pressure is still
close to 60 ). Given that eGFR should be measured at least annually in all
recorded as a common cause of end-
patients with high blood pressure , in
stage kidney disease ( ESKD ; ie , requiring dialysis or a transplant to survive or death due to kidney failure ), second
individuals with a ‘ normal eGFR ’ ( ie , eGFR greater than 60mL / min / 1.73m 2 ) observing the rate of decline of eGFR
equal with glomerulonephritis , with only diabetes causing more cases . 4 In Australia 12-14 % of patients who enter dialysis are reported as having hypertensive CKD . 12
So-called ‘ hypertensive nephropathy ’ is said to be higher in individuals with recent African and Indigenous ancestry . 13 , 14 Beyond the limited resources to exclude other causes , this association may partly reflect worse blood pressure control , as well as underlying susceptibility including genetic susceptibility ( eg , APOL1 mutation ), reduced nephron endowment , and toxin exposure ( eg , heavy metals
Figure 2 . Very high magnification micrograph of renal arterial hyalinosis in chronic / sclerosing allograft nephropathy ( periodic acid-Schiff stain ).
Nephron / CC BY-SA 3.0 / bit . ly / 4bAkAib
can also provide an early indication of progressive kidney disease . In particular , losses of 10mL / min / 1.73m 2 / three years or greater ( eg , eGFR falls from 80 to 70mL / min / 1.73m 2 over three years ) can be indicative of rapidly declining kidney function and warrants renoprotective intervention ( s ) detailed later .
Figure 6 provides an algorithm for initial detection and diagnosis of CKD .
CLINICAL PRESENTATION OF CHRONIC KIDNEY DISEASE
CKD is usually silent until the
and agrichemicals ). 4
PATHOPHYSIOLOGY
A healthy kidney is composed of mil-
advanced stages . 17 Patients with CKD will usually not experience kidney pain or changes in urine colour or output . Some individuals may notice an
lions of filtering units , known as
increase in nocturia , attributable to
nephrons ( see figure 1 ). Nephrons are
impaired nocturnal concentration
specialised structural units compris-
ability , although this will often be
ing a glomerular complex that filters
attributed to ageing bladder / prostate
the plasma , with a tubule running
functions or coincident diabetes .
from it that processes the filtrate and
Many patients with CKD will have a
defines the composition of the urine .
long ( er ) history of high blood pressure ,
High blood pressure can damage crit-
and manifest symptoms and signs
ical components of the nephron ,
high blood pressure . Tubular atrophy ,
volume expansion and neurohormonal
estimated by measuring the urinary
of longstanding high blood pressure ,
contributing to a progressive loss of
tubulointerstitial fibrosis and capillary
activation driving high blood pressure
albumin to creatinine ratio ( ACR ), as
including left ventricular hypertrophy ,
nephron integrity and kidney func-
rarefaction are the final common path-
and impairing responsiveness to treat-
the urinary creatinine adjusts for the
heart failure , oedema , atherosclerosis
tion . In particular , following chronic exposure to high blood pressure , the
way to nephron loss and replacement by scar tissue .
ment . In particular , CKD is associated with increased activity of the renin
void volume and urine concentration . 17 The first or second void in the morning
and hypertensive retinopathy . These may suggest a diagnosis of ‘ hyperten-
blood vessels that supply the nephron become thickened and the vascular
Taken together , these histopathological changes are known as ‘ arteriolar
angiotensin aldosterone system ( RAAS ) and sympathetic nervous system .
is generally considered best , but other voids ( eg , at a clinic visit ) can also be
sive kidney disease ’. As stated earlier , all these signs may also be present in a
lumen narrowed . Hyaline-like ( pink , amorphous , homogeneous ) material is exuded into the wall of preglomerular arterioles ( see figure 2 ). This is known as ‘ arteriolosclerosis ’. This process can progressively decrease glomerular blood flow and eventually lead to
nephrosclerosis ’ or ‘ nephroangiosclerosis ’ ( see figure 3 ); however , they are not specific or diagnostic of hypertensive kidney damage . Nephrosclerosis can also be observed in all of the most common forms of CKD , including diabetes , obesity , smoking , ageing and in
SCREENING FOR CHRONIC KID- NEY DISEASE IN PATIENTS WITH HIGH BLOOD PRESSURE
ALL people with high blood pres-
used for analysis without much loss of value . Regardless of the method , there is usually substantial day-today variability in the urinary albumin excretion rate . This means that any abnormal result should always be confirmed by undertaking two additional
patient with longstanding CKD , and it is almost impossible to tell which came first . In order to develop abnormal kidney function , more than half of the filtering nephron units must have been progressively lost over many years , during which time the kidney disease
ischaemic collapse and obsolescence
advanced stages of glomerulonephri-
sure require screening for CKD , at
samples over the next 3-6 months . If
may have adversely impacted on the
of the glomeruli . Equally , vascular
tis , in part due to remnant hyperfunc-
least annually , from the time of their
albumin excretion is within the nor-
patient ’ s blood pressure but the CKD
stiffening impairs healthy autoregulation of kidney blood flow , transmitting elevated systemic blood pressure to the delicate structures of the glomeruli , resulting in their remodelling and progressive dysfunction .
As kidney damage develops , the glomeruli are partly or wholly replaced by scar tissue ( known as focal , segmental or global glomerulosclerosis , respectively ). The extent of glomerular sclerosis correlates with the progres-
tion ( ie , the remaining nephrons carry a heavier burden leading to accelerated injury and progressive dropout ).
As the kidney has little or no regenerative capacity , once a nephron is lost , it cannot return . The remaining nephrons have substantial capacity to buffer losses in the short term . However , the extra workload that nephron loss creates acts to perpetuate further losses .
Reduced kidney function ( of any
diagnosis with elevated blood pressure . 15 The purpose of this screening is to identify those with high blood pressure in whom a different treatment ( kidney-protective ) strategy is needed to improve clinical outcomes . Screening encompasses the testing of both urinary albumin excretion rate and eGFR , as both are independently and additively associated with prognosis . 16 This is conceptualised in the Australian Kidney Health Check pro-
mal range in both tests , future screening can be repeated on an annual basis . If one or both urinalyses are abnormal , then a diagnosis of CKD can be recorded , and a new treatment plan initiated ( as detailed later ).
Urine dipstick tests ( to estimate urinary albumin or protein ) are not generally recommended . Although an elevated urine albumin concentration on a dipstick is almost always associated with an abnormal ACR , less than
was not diagnosed until their kidney function ultimately became abnormal .
DIAGNOSIS OF CHRONIC KID- NEY DISEASE IN PATIENTS WITH HIGH BLOOD PRESSURE
CONSIDER additional investigations in
any patient presenting with impaired kidney function to determine the
sive decline in kidney function , as well
cause ) progressively leads to endothe-
gram ( see figure 4 ). 17
half of those with an abnormal ACR
potential cause ( s ), optimal treatment
as other clinical features like secondary
lial dysfunction , sodium retention ,
Urinary albumin excretion is best
will be dipstick positive . 18
and likely prognosis .