Renal Diseases in Geriatrics

By – Dr Gaurav Singh
o STRUCTURAL CHANGES –
• GROSS
• MICROSCOPIC

o FUNCTIONAL CHANGES

o RENAL DISEASES
 STRUCTURAL CHANGES IN OLD AGE -
GROSS
• Renal mass, size , weight and volume decrease with normal aging.

• Kidneys reach maximum mass in 4th decade of life of upto maximum

400grams(both) and starts to decrease by 10% of its mass every decade to the
point that it weighs only 200grams in those 90 years of age.

• These changes appear to be age appropriate in conjunction with concurrent loss

in body surface area.

• Body surface area also tend to decrease after 4th decade of life in both men and
women
STRUCTURAL CHANGES IN OLD AGE -
MICROSCOPIC
• On microscopy, glomerulosclerosis and tubulointerstitial fibrosis was evident.
• Intervening insults and comorbid conditions hasten the gradual and progressive
senescence of the renal vasculature, glomeruli, tubules, and interstitium.

• Hypertension worsens sclerotic changes in the renal arteries. Increased fibrointimal and
medial sclerosis is present in cortical arteries at age 70.

• Interlobular and arcuate arteries of older kidneys show greater arteriolosclerosis.

• By age 70, ischemic changes, including lobulation of the glomerular tuft, increased
mesangial volume, and capillary collapse and obliteration, are present in the cortical
nephrons. Little cellular response is evident, with hyaline deposition in the residual
glomeruli.
• Peritubular capillary density is decreased, offering a reason for the lower concentrations
of pro-angiogenic vascular endothelial growth factors and increased expression of anti-
angiogenic thrombospondin.

• Basement membrane thickening and wrinkling in glomeruli and tubules along with renal
vasculature changes lead to progressive reduction and simplification of vascular
channels, shunting blood from afferent to efferent arterioles of the juxtamedullary
glomeruli.

• As glomeruli sclerose, tubular atrophy follows, with a decrease in size and number.

• Tubules atrophy to form distal diverticula that may lead to early renal cysts frequently
seen in older kidneys.

• Debris and bacterial accumulation in these structures may account for the increased
incidence of infection in aging individuals.
• Animal studies indicate that tubulointerstitial fibrosis may precede the development
of focal glomerulosclerosis and tubular atrophy.

• Morphometry in aging mice suggests greater tubulointerstitial fibrosis in males than

females.

• Aging rodents with accelerated apoptosis demonstrate interstitial inflammation

with fibroblast activation.

• Immunostaining showing adhesive proteins osteopontin and intracellular adhesion

molecule-1 (ICAM-1) as well as deposition of collagen IV
RENAL DISEASES IN AGING KIDNEY

• DISORDERS OF OSMOREGULATION

• ACUTE KIDNEY INJURY

• RENOVASCULAR DISEASE/HYPERTENSION

• GLOMERULAR DISEASE

• CHRONIC KIDNEY DISEASE

• URINARY TRACT INFECTION

• RENAL CYSTS
 DISORDERS OF OSMOREGULATION - HYPONATREMIA

• Common finding in geriatric adults, given their enhanced osmotic AVP release
and impaired ability to dilute urine.

• Aging-associated decreases in PG synthesis inhibit water

• Aggravated by use of thiazide like diuretic use.

• Manifest as apathy, disorientation, lethargy, muscle cramps, anorexia, or nausea.

• Progress to more devastating signs such as agitation, depressed deep tendon

reflexes, pseudobulbar palsy, and seizures
DISORDERS OF OSMOREGULATION - HYPERNATREMIA

• Impaired concentrating defect and decreased thirst response with aging predispose
older individuals to dehydration and hypernatremia

• Inability to access free water (altered level of consciousness or immobility) can lead
to a marked rise in serum sodium and osmolality, with associated mortality
reported as high as 46%-70%.

• Medications that cloud sensorium and inhibit thirst, (tranquilizers and sedatives),
or that decrease AVP action in the renal tubules, such as (lithium,demeclocycline)
should be used with caution in older adults.
• In addition, osmotic diuretics, high-protein or high glucose parenteral feedings, and
bowel cathartics need to be used carefully in older adults to avoid dehydration.

• Systemic illness, fever or neurologic impairment may add to impaired AVP secretion
and increase the underlying predisposition for hypernatremia.

• Severe cellular dehydration can be associated with obtundation, stupor, coma,

seizures, and death.
 ACUTE KIDNEY INJURY
• Acute kidney injury is 3.5 times more prevalent in those older than 70 years

• Associated with greater morbidity and mortality in older hospitalized patients.

• 28% of those older than 65 years are unlikely to recover kidney function after AKI.

• In slices of kidney from older rats, expression of candidate genes, including claudin-7
(Cldn7), kidney injury molecule-1 (Kim-1), and matrix metalloproteinase (MMP-7), was
increased during ischemic injury in comparison with younger rats.

• Interestingly, gene expression was attenuated in calorie restricted older rats

• The common presence of comorbid diabetes, hypertension, heart failure, liver disease,
or malignancies in older individuals adds to the poor tolerability of an acute renal insult.

• Approximately half of the AKI events in the elderly result from prerenal processes.

• Vomiting, diarrhea, bleeding, and excessive diuretic use are common causes of
dehydration and volume depletion in this population.

• Impaired thirst, decreased urinary concentration ability and diminished sodium

conservation capacity predispose to these processes.

• Blunted autoregulation, decreased RPF, and reduced renal reserve in the older kidney
allow volume changes to be less well tolerated.
• Evolution from prerenal azotemia to acute tubular necrosis (ATN) occurs more commonly
in older (23%) than younger (15%) patients.

• ATN from ischemic and nephrotoxic tubular injury affects approximately 50% of
hospitalized older patients with intrinsic AKI.

• Lower levels of the NO substrate, l-arginine, in the elderly are associated with decreased
NO synthesis in aging vasculature and higher ADMA levels, impairing vasodilation and
predisposing older kidneys to ischemia

• Hypotension, either before or after surgery, sepsis, and nephrotoxins are poorly tolerated
by aging kidneys and are major culprits in hospital-acquired AKI in the elderly.

• Nephrotoxins contributed to AKI in 66% of the elderly patients, sepsis and hypotension in
45.7%, contrast-induced nephropathy in 16.9%, and postoperative renal failure in 25.4%,
with various combinations of these factors leading to AKI
• Drug-induced interstitial nephritis is more common in the elderly, particularly with
commonly used drugs such as penicillins and proton pump inhibitors.
Both decreased clearance and tubular changes in older kidneys predispose to the
toxic effects of antibiotics, chemotherapeutics, and diagnostic agents such as those
using
iodinated contrast.

• Whenever possible, diuretic agents should also be discontinued several days prior to
contrast agent injection

• Analysis of murine kidney tissue in experimental AKI suggested that TNF–like weak
inducer of apoptosis (TWEAK) activation of its receptor, fibroblast growth factor–
inducible 14 (Fn14), via secretionof chemokine CXCL16 decreased both mRNA and
protein expression of the anti-aging hormone Klotho.
• Atheroembolic AKI is of greater risk in elderly patients who have generalized
atherosclerosis.

• In one study, 7.1% of renal biopsy specimens obtained for AKI in patients older than
60 years were found to have atheroemboli.

• Subtle increases in blood urea nitrogen and creatinine with or without complaints of
dysuria, hesitancy, or dribbling should prompt an evaluation for underlying urinary
tract obstruction.

• Careful investigation for urogenital tumors, pelvic prolapse, and papillary

sloughing, , medication review for anticholinergic drugs, sedatives and hypnotics,
narcotic and opioid analgesics, antipsychotics, and histamine-1 receptor antagonists,
should be considered, with prompt urologic intervention.
 RENOVASCULAR DISEASE
• Renovascular disease is cause of resistant hypertension and progressive renal insufficiency,
manifesting in the elderly as part of a generalized atherosclerotic process rather than an
isolated syndrome .
• Incidence of 1.3% and prevalence of 0.7% of ESKD is in those, diagnosed with atherosclerotic
renovascular disease (ARVD)
• The prevalence of renovascular disease has been estimated to be 6.8% in community-
dwelling men and women older than 65 years.

• Unexplained progressive azotemia, worsening or new-onset hypertension, or development

of AKI with antihypertensive therapy should raise suspicion of renovascular disease in an
elderly patient.
• These signs may be more evident when ACEI and ARBs are used
• Patients with ARVD are at increased risk of death from CVD; therefore, aggressive control of
atherosclerotic risk factors is recommended.

• Treatment for hemodynamically significant lesions, including medical therapy with

antihypertensive drugs, revascularization with angioplasty with or without stenting, and
surgery, should be individualized with consideration of the benefits and risks of each.

• A randomized trial comparing endovascular revascularization plus medical therapy with

medical therapy alone in 806 older patients with ARVD found no clinical benefit for
revascularization when the end points of renal function, blood pressure, time to renal and
cardiovascular events, and mortality were assessed over 34 months of follow-up.

• Revascularization also carries the risk of atheroemboli.

• There is no evidence that revascularization improves any outcomes in asymptomatic

patients.
 CHRONIC KIDNEY DISEASE
• CKD increases in prevalence with age & is present in 38% of U.S. adults 70 years & older.
• CKD with eGFR less than 60 mL/min/1.73 m2.
• Frailty is also more prevalent among older patients with CKD & cognitive impairment
increases in older CKD patients independently of other confounding factors.

• AKI can hasten the progression of CKD (secondary to medical disease such as diabetes,
hypertension, chronic GN, renovascular and obstructive nephropathy)

• Prolonged use of analgesics, seen in the elderly, may be associated with papillary
necrosis and progression to CKD.

• Older individuals may experience episodes of volume overload and symptoms of heart
failure, gastrointestinal bleeding, hypertension, or gradual confusion that indicate
progression of renal loss
• CKD in the elderly is associated with a greater risk of kidney failure, CVD, CVA and
death.

• Interestingly, the most common cause of death in elderly patients with CKD is CVD
rather than the progression of kidney disease to kidney failure

• Therefore, cardiovascular risk management remains important in elderly patients with

CKD.

• Estimates of renal function from serum creatinine levels alone may be inadequate in
the elderly; For estimating GFR in the elderly continues, MDRD and CKD-EPI equations is
preferred.
 URINARY TRACT INFECTION
• Common and a frequent reason for hospital admission
• Weakened host defense mechanisms, age-related mechanical and hormonal changes
lead to urinary tract obstruction or urine stasis which promote UTI
• Bladder dystonia, pelvic musculature changes, prostatic enlargement, and urethral
stricture can cause obstructive uropathy.
• Decreased prostatic secretions in older men may predispose to infections of the
lower urinary tract. Prostatic microcalculi can harbor bacteria and become a nidus for
infection in an elderly man.
• Decreased vaginal estrogen levels in postmenopausal women lead to reduced
lactobacilli and raise the risk of infection.
• Indwelling urinary catheter use in elderly, might cause bacterial colonization and
biofilm formation and is associated with UTI.
• The incidence of asymptomatic bacteriuria increases with rising age

• As asymptomatic bacteriuria does not necessarily predict poor outcome/treatment

effect on morbidity/mortality in the elderly, routine screening/treatment of
asymptomatic bacteriuria, +/- pyuria, is not recommended for either community-
dwelling or institutionalized elderly.
• For elderly patients without indwelling catheters, the minimum criterion for antibiotic
therapy is
acute dysuria alone or fever, in the presence of at least one of the following:
new or worsening urgency,
frequency, suprapubic pain,
gross hematuria,
costovertebral angle tenderness, and
urinary incontinence.

• For treatment of symptomatic infection, antimicrobial should be delayed, wherever possible,

until culture results are available.

• For symptomatic infection with an indwelling catheter, the catheter should be removed and
replaced with a new catheter before initiation of antimicrobial treatment. Escherichia coli
remains the most common cause of symptomatic UTI in older men and women
• Treatment is continued for 10 to 14 days for pyelonephritis in both men and women.

• Duration of therapy in men is usually 7 days for cystitis.

• Chronic bacterial prostatitis is usually associated with recurrent UTIs. Initial treatment
with a prostate penetrating antimicrobial agent (fluoroquinolone/cotrimoxazole) is
effective.(or as per cultures). The usual course of therapy is 4 weeks

• Long-term (6- to 12-month) low-dose prophylactic antimicrobial therapy is used for

prevention of recurrent uncomplicated UTI in older women who are experiencing two or
more UTI episodes in a 6-month period. A first-line regimen is nitrofurantoin 50/100 mg
or cotrimoxazole, one half a regular strength tablet daily or every other day at bedtime
 RENAL CYSTS
• Simple renal cysts are common in aging kidneys,
• Benign, asymptomatic and usually are incidental findings.
• Solitary or multiple, bilateral and generally have little clinical significance.
• Relative frequency of 2 : 1 in men compared with women.
• Prevalence - 11.5% in individuals aged 50 to 70 years and
22.1% in those aged 70 years
36.1% in those aged 80 year or above
• Cysts with smooth clear walls and are fluid filled without internal echoes require no further
workup.
• However, a cyst that is filled with debris or internal echoes, thick walled, or occurs in
association with a possible renal mass is considered complicated and needs thorough
workup.
THANK YOU