Genitourinary Disease

Age Changes



1. In old age, renal function is reduced to about 50% of the peak at 30 years.

2. Serum urea may remain in the normal range despite deteriorating renal function.

3. Creatinine reflects muscle bulk; so beware the frail elderly patient with a ‘normal’ level of creatinine.

4. The estimated glomerular filtration rate (eGFR) can be calculated using the creatinine, gender and age. This only applies in steady states, not in acute deterioration.

5. Ability both to concentrate urine and to process an extra water load quickly is impaired. This is one explanation for nocturia in old age. Maximum urine concentration falls from 1300 to 850 mOsm/L.

6. There is loss of renal mass, affecting the cortex more than the medulla, in half of ‘normal’ elderly kidneys.

7. Reduced renal function is due to:

  • Loss and sclerosis of glomeruli leading to fewer functioning nephrons.
  • Reduced renal blood flow, particularly to the cortex.
  • Diminished response to antidiuretic hormone (ADH).

These effects are exaggerated in hypertension, diabetes and after pyelonephritis.

8. The combination of ageing changes and systemic or renal disease may lead to rapid, dramatic deterioration in renal function.

9. Atrophic changes occur in the urogenital tract of post-menopausal women as oestrogen levels fall.

10. Prostate size increases and cancerous foci become common.

11. The incidence of unstable bladder increases due to sudden uncontrollable surges in bladder pressure secondary to contractions whilst filling (detrusor instability).

Acute Kidney Injury (AKI) in Old Age


AKI is now the preferred term for acute renal failure. AKI is defined as an abrupt rise in serum creatinine, usually accompanied by a decrease in urine output. AKI is common in older people admitted to hospital, but is also a frequent complication during admission (in up to 20% of cases). The ageing kidney does not have sufficient reserve to tolerate insults such as dehydration and sepsis; AKI is usually multifactorial and iatrogenic factors such as drugs and inadequate fluid management often contribute. Pre-existing renal damage from hypertension and diabetes, cardiovascular co-morbidity and poor nutrition increase the vulnerability of old kidneys to common acute insults. As the outcome of AKI is poor in old age, identifyat-risk patients and manage them carefully to prevent AKI.


Causes


See Table 13.1.


Table 13.1 Causes of acute kidney injury in older people
































Pre-renal Renal Post-renal
Dehydration Acute tubular necrosis results from ischaemia (usually from a pre-renal cause) Prostatic hypertrophy
Blood loss Nephrotoxins, e.g. drugs, contrast agents Ureteric stones
Pump failure Myoglobinuria secondary to rhabdomyolysis (falls) Prostate cancer
Over-treatment of hypertension Allergic interstitial nephritis Gynaecological cancer
Sepsis (vasodilation) Systemic diseases – myeloma, gout, etc. Bladder cancer
Renovascular disease Glomerulonephritidies Retroperitoneal fibrosis

History



  • Evaluate for all causes of volume depletion and hypotension (e.g. poor oral intake, vomiting, diarrhoea, GI bleed, sepsis, over-diuresis, ACS and antihypertensives).
  • New onset postural dizziness suggests volume depletion.
  • Ask about all drugs including over-the-counter (OTC) herbal preparations as some cause allergic interstitial nephritis.
  • Confused, elderly inpatients may not drink enough, and may be given medications (including diuretics, ACEi) that they had stopped taking at home long ago.
  • Lower urinary tract symptoms (LUTS).
  • Past medical history: prostate, bladder and ovarian, cervical or uterine cancer.
  • Review previous blood results to check baseline function.

Examination



  • Assess fluid status (patients with oedema can still be intravascularly depleted).
  • Check lying and standing blood pressures and heart rate. A postural drop and tachycardia indicate hypovolaemia.
  • Check the jugular venous pressure (JVP) carefully.
  • Palpable bladder?
  • Rectal examination; size and character of the prostate.

Investigations



1. Urgent electrolytes: hyperkalaemia is the most immediately life-threatening abnormality.

2. Hypernatraemia is common in severe dehydration with drowsiness leading to poor oral intake; prognosis is very poor.

3. ECG to check for effects of hyperkalaemia (see Figure 13.1).

4. FBC, CRP and ESR to check for sepsis or inflammation. Normocytic anaemia may indicate CKD.

5. Urea and creatinine.

6. Glucose/HbA1c.

7. Bone profile – high phosphate suggests CKD.

8. ABG and lactate – ?acidotic.

9. CXR: cardiomegaly, pneumonia, pulmonary oedema and infiltrates (vasculitis).

10. Ultrasound: assess for bladder outflow obstruction, hydronephrosis and also kidney size (if small, suggestive of chronic renal disease).

11. Urinalysis: leucocytes and nitrites suggest infection; blood and protein suggest renal disease.

12. Midstream urine (MSU): microscopy for casts and culture.

13. Further tests, guided by the results of the above, might include creatine kinase, protein electrophoresis and Bence–Jones protein, uric acid, autoantibodies, CT scan.


Figure 13.1 ECG in hyperkalaemia. Source: Wikimedia Commons (public domain).

img

Management



1. Treat hyperkalaemia: intravenous calcium gluconate first (10% in 10 mL aliquots by slow push) and then 50 mL 50% dextrose with 10 units of insulin over 20 min.

2. Fluid resuscitate: if in doubt, give 250 ml 0.9% saline stat, review and repeat as needed.

3. Catheter to relieve urinary obstruction and to monitor urine output.

4. Antibiotics for sepsis.

5. Stop nephrotoxins, especially NSAIDs and diuretics, ACEi, ARBs plus other antihypertensives if the patient is dry or hypotensive. Check ALL drugs on the chart in the BNF – do not rely on your memory.

6. Reduce the dose of drugs metabolized by the kidneys, e.g. enoxaparin.

7. Daily weight helps guide fluid balance.

8. A nephrostomy tube inserted under ultrasound guidance reduces unilateral hydronephrosis. If this is secondary to a stone blocking the ureter, the patient is referred to urology for insertion of a J-J stent. If the hydronephrosis is secondary to tumour, it may be more appropriate to leave the nephrostomy in situ for symptomatic relief.

9. Refer to nephrology for advice, consideration of temporary haemofiltration (to allow acute tubular necrosis to resolve) and longterm renal replacement therapy. Age alone is not a contraindication to dialysis. However, co-morbidities such as low output heart failure make haemodialysis challenging.

Complications



  • Acidosis.
  • Hyperkalaemia.
  • Oedema.
  • Sepsis.
  • Respiratory failure.
  • Encephalopathy.
  • Haemorrhage.

Chronic Kidney Disease (CKD) in The Elderly



  • Observe caution when interpreting creatinine because older people tend to have a lower muscle mass and therefore a lower creatinine level whatever the renal function.
  • CKD is diagnosed using eGFR which is based on the MDRD (Modification of Diet in Renal Disease) calculation.
  • CKD is common – 70% of > 70 year olds have CKD 3 – this reflects vascular disease and renal ageing; these patients are more likely to die from vascular disease than kidney failure.

Causes







Common causes of CKD in older people


1. Diabetes mellitus

2. Hypertension

3. Obstructive uropathy

4. Chronic pyelonephritis

5. Cardiac insufficiency

6. Renovascular disease

7. Myeloma

8. Systemic vasculitis

Biopsy is rarely helpful if the kidneys are small.






Symptoms


Table 13.2 shows the stages of CKD. Symptoms appear usually only in CKD 4/5 – poor appetite, nausea and vomiting, tiredness, breathlessness, peripheral oedema, itch and cramps.


Table 13.2 Stages of CKD




























Stage Description eGFR (mL/min/1.73 m2)
1 Normal or increased eGFR ≥ 90
2 Mildly decreased eGFR 60–89
3 Moderately decreased eGFR 30–59
4 Severely decreased eGFR 15–29
5 Kidney failure < 15

Signs


Assess fluid balance to exclude hypovolaemia due to infection, dehydration or overload; palpable bladder, enlarged prostate or uraemic frost (anaemia plus uraemia).


Investigations


As for AKI. Look for anaemia (decreased epo production from renal fibroblasts) and renal bone disease (increased PTH due to deficient 1α hydroxylation of vitamin D in proximal tubule mitochondria and phosphate retention).


Management



  • The objectives are to prevent progression, reduce complications, treat cardiovascular risk factors and control symptoms. If there are no contraindications use aspirin or simvastatin; target BP < 138/80 if possible without inducing symptomatic postural hypotension.
  • The best drugs to reduce blood pressure and proteinuria are ACEi and ARBs, but they reduce renal blood flow and may worsen renal function if the patient is hypovolaemic. Start with a small dose and monitor!
  • Fluid retention may need high dose loop diuretics with cautious use of metolazone watching the potassium.
  • Review medications, reducing doses and monitoring levels where appropriate. See ‘Drugs and the kidney’ below.
  • Erythropoietin injections/iron infusions for symptomatic anaemia.
  • 1α calcidol/phosphate binders (Calcichew, sevelamer).
  • Renal diet (low sodium, potassium and phosphate) is often unpalatable, and not necessary for end-of-life patients.
  • Education regarding diet, regulating fluid intake and concordance with medications.
  • Renal replacement therapy: in the UK 46% of dialysis patients are aged over 65 and 33% are aged over 70 years.
  • Many elderly patients adopt a philosophical approach, which makes them suitable for continuous ambulatory peritoneal dialysis (CAPD).
  • Palliative care when needed.






Complications of CKD

Renal osteodystrophy


Hypocalcaemia

Hyperphosphataemia

Secondary hyperparathyroidism (increased PTH)

Cardiovascular: increased risk of stroke, amputation, MI


Hypertension

Atherosclerosis

Anaemia

Metabolic acidosis

Malnutrition: secondary to anorexia, renal diet, increased protein catabolism





Intrinsic Renal Disease


Specific kidney diseases are less common than pre- and post-renal causes of renal failure in elderly patients.



  • Nephrotic syndrome. In a series of patients aged over 50 (diabetics were excluded), the underlying cause in order of incidence was:


img Membranous glomerulonephritis.

img Proliferative glomerulonephritis.

img Amyloid: usually secondary to long-standing inflammatory disease, e.g. bronchiectasis, osteomyelitis or rheumatoid arthritis.

img Minimal-change glomerulonephritis.


  • Diabetic nephropathy – common, no special features in old age.
  • Hypertensive damage – common.
  • Myeloma: see Chapter 14.
  • Nephrocalcinosis/stones. Exclude excess vitamin D, gout and hyperparathyroidism, all more common in old age.

Urinary-Tract Infection (UTI)



  • Very common in old age: 20% of people over the age of 65.
  • This increases to 50% of women in institutional care.
  • Female-to-male ratio: 3:1.
  • Escherichia coli is the most common pathogen. Others include Proteus mirabilis, Pseudomonas and Klebsiella.
  • Catheter-related infections are hard to eliminate unless the catheter is changed.
  • Asymptomatic bacteriuria with no pyuria does not require treatment.
  • Pyelonephritis is responsible for 20% of cases of renal failure.


Precipitating factors for UTI in old age are:




1. Urinary stasis:

  • Incomplete voiding.
  • Outflow obstruction, including constipation.
  • Increased bladder diverticula, e.g. secondary to BPH.

2. Loss of acidity of the female urethra, atrophic vaginitis and urethritis due to reduced oestrogen.

3. Associated disorders:

  • Diabetes.
  • Immobility.
  • Indwelling catheter.
  • Poor fluid intake.

4. Urinary-tract stones.

Presentations of Urosepsis in Old Age



1. Increased frequency and dysuria are common, but there may be other vague symptoms such as nausea, vomiting and lethargy.

2. Delirium: catheterization may be required to obtain specimen; alternatively organisms may be isolated from a blood culture. NB: UTI is rarely the sole cause of the delirium!

3. New urinary incontinence; infected urine irritates the bladder mucosa.

4. Increasing drowsiness due to worsening renal impairment.

Management


Aug 6, 2016 | Posted by in GERIATRICS | Comments Off on Genitourinary Disease

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