Renal & Urinary Disorders

NT4_2017-18

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 Learning Objectives
• To list the physiology and the functions of the renal and
urinary system (self study)
• To explain the etiology and the investigations of the
common renal and urinary disorders
• To understand the assessment of renal and urinary
disorders
• To explain the laboratory findings according to the
different states of renal disorders
• To define the treatment plan for renal failure

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 Functions of the Kidney
1. Regulation of extracellular fluid volume (ECF)
ECF is an important determinant of blood pressure
2. Regulation of blood osmolarity
3. Maintenance of electrolyte balance
4. Regulates blood pH
5. Excretes waste
6. Hormone production

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 How the kidneys form urine?
Nephron is the functional unit of the kidney
Urine is formed by filtration in the glomerulus
• Step 1: Glomerular filtration
Reabsorption of Na and glucose, osmosis then causes
water reabsorption
• Step 2: Tubular reabsorbtion (proximal convoluted
tubule ~ 80% resbsorbtion)
Na, K and glucose reabsorption, antidiuretic hormone
causes water reabsorption
• Step 3: Tubular secretion (distal convoluted tubule)
Ammonia and hydrogen (active transport)
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 Ali & Gray-Vickrey, 2011

Copyright © 2013 Nursing2013. Published by Lippincott Williams & Wilkins. 5

 Hormones & the urinary system (1)
Urine concentration is controlled by the
hypothalamus and the posterior pituitary gland.
Antidiuretic hormone (ADH) secreted by the
posterior gland, regulates levels of urine output.
High levels of ADH increase water absorption and
urine concentration.
Low BP, low blood flow and low levels of serum
Na passing through the kidneys that stimulates
the kidneys to release renin. That means to
activate renin-angiotensin-aldosterone system
(RAAS). 6
 What is RAAS ?
Renin is an enzyme that’s secreted by the kidneys
(juxtaglomerular apparatus).
It leads to the formation of the hormone called
angiotensin I. As it circulates through the lungs,
angiotensin I is converted into angiotensin II by
angiotensin-converting enzyme. Angiotensin II exerts a
powerful constricting effect on the arterioles, so that it
can raise blood pressure.
Angiotensin II stimulate the release of aldosterone.
Aldosterone is produced by the adrenal cortex. It
promotes Na reabsorption in the collecting ducts,
thereby raising BP.
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 Hormones & the urinary system (2)
Erythropoietin is a protein produced in the
kidney. It promotes red blood cell formation in
bone marrow.
Vitamin D is a steroid hormone metabolized in
the kidney to the active form 1,25-
dihyroxycholecalciferol, which promotes calcium
and phosphate absorption from the gut as a
principal action.

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 What is Creatinine?
Creatinine is a waste product from the normal
breakdown of muscle tissue. As creatinine is
produced, it's filtered through the kidneys and
excreted in urine.
The kidneys' ability to handle creatinine is
called the creatinine clearance rate, which
helps to estimate the glomerular filtration rate
(GFR) -- the rate of blood flow through the
kidneys.
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Measuring GFR – Creatinine Clearance Rate
Glomerular Filtration Rate (GFR) is the index of renal
function, but it can’t be measured directly.
Creatinine clearance in a healthy young person is
about 125 milliliters per minute -- meaning each
minute, that person's kidneys clear 125 mL of blood
free of creatinine
Falling GFR = progressing disease
Plasma Creatinine often taken as indicator of renal
function, but GFR is normally the best!
GFR = Creatinine Clearance = Urine conc. x Urine flow rate
Plasma conc.
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 National Kidney Foundation (NKF)
recommendation
• In adults, the level of GFR should be estimated
by the MDRD and Cockroft-Gault equations
• 24-hr urine sample is, however, advisable in
individuals with exceptional dietary intake
(e.g. vegetarian diet) or muscle mass (e.g.
amputation, gross malnutrition)
 http://www.kidney.org/professionals/KDOQI/gfr_calculator

Materials adopted from Dr Bonnie KWAN, Hong Kong Society of Nephrology

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O’Callaghan, 2009
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 Renal & urological assessment (1)
History taking
 Chief complaint
 Symptom analysis
– Disturbances in urination
– changes in urinary volume
– Irritative manifestations: urinary frequency;
urgency; nocturia; dysuria
– Obstructive manifestations: hesitancy; straining to
begin urination; intermittency; decreased force &
caliber of urinary stream; high post void residual;
and urine retention (acute or chronic).

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 Renal & urological assessment (2)
Urinary incontinence: urge; reflex; stress; mixed;
overflow; and functional
Alterations in urine characteristics: color; clarity; odor
Pain or Referred Pain
Systemic Manifestations

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 Renal & urological assessment (3)
Past health history
Childhood and infectious diseases
Trauma
Major illnesses and Hospitalizations
Operations
Medications
Allergies

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 Renal & urological assessment (4)

Family health history

Psychosocial history
Occupation
Geographical location
Exercise
Nutrition* (Tainted milk formula)
Habits* (teenagers’ recreational drug use)

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 Diagnostic investigations

• Renal scan • Ultrasound

• Renal biopsy • CT scan
• Renal • MRI
Arteriography

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 Renal biopsy
Three reasons
1. Establish the exact diagnosis
2. Determine therapy
3. Prognosis: degree of active (potentially
reversible) and chronic (Irreversible) changes

Materials adopted from Dr CHOW Kai-ming / PWH 20

 Renal biopsy technique
• Ultrasound real-time guidance with LA
• Localise desired lower-pole site ( at which the
risk of puncturing a major vessel is minimized)
• Determine renal size and detect unexpected
presence of cysts
• Patient must hold breath during the test

Materials adopted from Dr CHOW Kai-ming / PWH 21

 Urinary Tract Infection (UTI)
Cystitis (Inflammed bladder)
Pyelonephritis (Kidney infection)
Urethritis (Infection of urethra)
Ureteritis (Infection of ureter or ureters)
 The ureter rarely is infected alone, but there is either a pyelonephritis or a cystitis
associated with it
Prostatitis (Infection of prostate)
Investigations:
urine testing, urine for culture & sensitivity, blood tests if systemically
unwell,
ultrasound, X-ray of kidneys, ureters & bladder (KUB),
Intravenous urogram/pyelogram (IVU / IVP)
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 Urinary Tract Infection (cont’d)
 Causes:
 E-coli is the main organism (>70% in the community
but ≤ 41% in hospital).
 Risk Factors:
 Sexual intercourse, pregnancy, menopause,
immuno suppression, catheter-associated and
nosocomial infection.
 Treatment:
• Analgesic – Pyridium (urine turned to bright orange
in color) - ↓spasm and ↓pain
• Antibiotics – Septra, Levofloxacin, Cefuroxime,
Ciprofloxacin 23
 Prevention of UTI

 Drink plenty of fluids

 Cranberry juice or lingonberry juice (Kontiokari et al., 2001)
 Void frequently and completely
 Personal hygiene
 Woman: void after intercourse to help prevent
urethral infection

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 Parts of urinary tract affected Signs & symptoms

Kidneys (acute pyelonephritis)  High fever

 Rigors
 Vomiting
 Loin pain and tenderness
 Oliguria (if ARF)

Bladder (cystitis) or lower UTI  Dysuria

 Frequency
 Urgency
 Suprapubic pain or tenderness
 Hematuria

Prostatitis (prostate)  Flu- like symptoms

 Low backache
 Few urinary symptoms
 Swollen or tender prostate on PR

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 Characteristics of urine & organisms
Urine Organisms
• Protein Gm –ve
• Blood • E-coli
• Klebsiella
• White cells
• Proteus
• Bacteria
• Usually cloudy, Gm +ve
offensive smelling • Staphylococcus
saprophyticus (with
sexual activity) 26
 Characteristics of urine
• Urea nitrogen
- Concentration of urea in the blood, regulated by the
rate at which the kidney excretes urea
• Urine specific gravity
- Indicates the concentrating ability of the kidneys, high
specific gravity indicates dehydration
• Urine osmolarity (more accurate than gravity)
- Determines the diluting and concentrating ability of
the kidneys

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 Hematuria
Glomerular Extra-glomerular
• Structural disruption of • Site: lower urinary tract
glomerular basement - Ureter, bladder, urethra
membrane • Cause:
- IgA nephropathy - Trauma
- Lupus nephritis - Stones (calculi): mechanical
- Thin membrane disease erosion of mucosal surfaces
- Alport’s disease - Tumours
- Chemicals: toxic disruptions
of the renal tubules

Materials adopted from Dr Bonnie KWAN, Hong Kong Society of Nephrology

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 Proteinuria
Glomerular Non-glomerular
• Primary • Transient
- Membranous GN - Acute illness
- Minimal change GN - Pregnancy
- IgA N - Vaginal discharge
- FSGS - Menstruation
- Mesangioproliferative GN - Diet (beetroot)
• Secondary • Persistent
- Vasculitis - Orthostatic
- DM - Non-renal
- Lupus - Tubular
- Amyloidosis - Overflow
- Myeloma
Materials adopted from Dr Bonnie KWAN, Hong
- Hepatitis B or C Kong Society of Nephrology
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 Other Urinary & Renal Disorders
Renal calculi
Glomerulonephritis
Nephrotic Syndrome
Diabetic nephropathy
Polycystic kidney disease
Renal tract cancer
Acute renal failure
or acute kidney injury (AKI)
Chronic renal failure
or chronic kidney disease (CKD)
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 Urolithiasis & Nephrolithiasis
(Renal calculi)
Renal stones consists of crystal aggregates (~75% calcium
oxalate). Uric acid stones is a metabolic product of purines.

Signs & symptoms:

 Maybe asymptomatic
 Loin pain (stones in the kidney) or from “loin to the groin”
 Stones in the ureter cause renal (ureteric) colic.
 Bladder or urethral stones cause pain in micturition,
strangury or interruption of urine flow.
 May be infection, hematuria, proteinuria etc.

Test: urine test, KUB, ultrasound, intravenous pyelogram (IVP)

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 Intravenous PyeIogram (IVP)

In the procedure intravenous pyelogram (IVP), the patient is injected with

radiopaque dye and X-rays are taken as the dye travels through the urinary
tract. This procedure is performed to confirm the presence of kidney stones,
although some stones may be too small to see.

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 Renal calculi (cont’d)
Treatments:
• Allopurinol (Zyloprim) – prevent uric acid stone formation
• Analgesic – ibuprofen, morphine: ↓spasm & ↓pain
• Antibiotics if infection

Endourological Procedures:
 Extracorporeal Shock Wave Lithotripsy (ESWL)
 Percutaneous nephrolithotomy (PCNL)

Open Surgical Procedures:

 Pyelolithotomy, Nephrolithotomy, Ureterolithotomy &
Cystolithectomy

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 Ureteral Stent
A ureteral stent maybe
used:
 To bypass a blockage in
a kidney or ureter
 During kidney stone
removal
 To let a ureter heal after
sugery

Source: http://www.uro-docs.com/ureteral-stents/ 34
 Extracorporeal Shock Wave Lithotripsy (ESWL)

It used to shatter simple stones in the kidney or upper urinary tract. Ultrasonic waves are passed
through the body until they strike the dense stones. Pulses of sonic waves pulverize the stones,
which are then more easily passed through the ureter and out of the body in the urine.

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During a PCNL, the surgeon inserts a needle through the patient's back directly into the
kidney (B). A nephroscope uses an ultrasonic or laser probe to break up large kidney stones
(C). Pieces of the stones are suctioned out with the scope, and a nephrostomy tube drains
the kidney of urine (D).
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Percutaneous nephrolithotomy (PCNL)
 Prevention of renal calculi

Drink plenty of fluid (aim 2-3L/day of colorless urine)

Normal calcium intake is now recommended (low
calcium diets increase oxalate excretion)
Less tea, chocolate, nuts, rhubarb and spinach
(increase oxalate levels)
Avoid organ meats and meat extracts (food high in
purine)
If the renal calculi of calcium phosphate composition,
you should take low calcium and low phosphate diet.

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 Care of patient with
Percutaneous Nephrostomy Tube (PCN)
Aims:
1. to create temporary or permanent urinary diversion, to
relieve obstruction from an inoperative tumor, or
provide an outlet for urine after cystectomy.
2. A temporary diversion can relieve obstruction from a
calculus or ureteral edema

Care of the PCN: simple dressing is required like the

drain care.
Irrigating of the PCN: usually performed by physician

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 Glomerulonephritis (GN)
 It is a bilateral inflammation of the glomeruli,
commonly following a streptococcal infection like
respiratory tract infection.
 It can be acute or chronic.
 Kidney biopsy is typically used to identify the type of
glomerulonephritis.
 Primary GN – immune response to pathogens, i.e.
postinfectious GN, IgA nephropathy etc.
 Secondary GN – related to systemic disease like SLE

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 5 Clinical syndromes of glomerular disease

Asymptomatic proteinuria or hematuria

- result from mild glomerular damage
Acute glomerulonephritis (Nephritic Syndrome)
- consists of hematuria, ↓GFR, Na and water
retention & hypertension
Chronic glomerulonephritis
- consists of slow progressive glomerular damage,
often with proteinuria, hematuria & hypertension
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5 Clinical syndromes of glomerular disease
(cont’d)
Rapidly progressive glomerulonephritis
- A syndrome of rapid renal failure
- Oliguria, hematuria & proteinuria
- Usually without other features of the Nephritic
Syndrome
Nephrotic Syndrome
- Heavy proteinuria, leading to hypoalbuminemia
& edema
O’Callaghan, 2009
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Glomerular Disease : An overview

O’Callaghan, 2009
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Nephritic syndrome vs Nephrotic syndrome

Nephritic Nephrotic
• Hematuria (red or • Proteinuria (urine may be
brown urine) frothy)
• edema & generalized • Hypoalbuminemia
fluid retention • edema & generalized fluid
• Hypertension retention
• Oliguria • Intravascular volume
• variable proteinuria depletion with hypotension,
or expansion with
hypertension, may occur
• variable haematuria 44
 Nephrotic Syndrome
 classical triad of heavy proteinuria
Urinary excretion of ≥ 3.5g of protein /day in adults or
> 40mg/m2/hr in children
Hypoalbuminemia of < 30g/L in adults or < 25g/L in
children
edema

N.B. Hypercholesterolemia is common

Diagnosis is by measurement of a spot urine
protein/creatinine ratio or a 24-h urinary protein
Materials adopted by Dr CHOW kai-ming / PWH

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 Pathophysiology of Nephrotic Syndrome
↑ in glomerular permeability

↑ filtration of plasma protein

Loss of Ig / complement
Loss of anticoagulant Loss of albumin

↓ albumin Infection
↑ tubular
Thromboemoblism absorption

↑ lipoprotein
Tubular synthesis
dysfunction Edema

Hyperlipidemia

Materials adopted from Dr CHOW Kai-ming / PWH 46

O’Callaghan, 2009
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 Approach to nephrotic syndrome
Principle: always a glomerular disease
• In children, 90% due to minimal change
nephropathy, so give a trial of steroid; renal
biopsy only if there is atypical feature, or if the
child responds poorly
• In adults, renal biopsy is indicated unless the
diagnosis is immediately obvious

Materials adopted from Dr CHOW Kai-ming / PWH 48

 General management of nephrotic syndrome
Monitor I/O, BP, body weight regularly to treat edema
 Salt intake and fluid intake restriction
 loop diuretics (Lasix IV**) ± thiazide-type diuretics
(spironolactone) on alt. day to promote diuresis
 Requires daily body weight measurement, aiming for
0.5-1kg weight loss/day
 Protein restriction to 0.8g/kg/day
 Anti-proteinuric drugs, i.e. ACEI or ARB (administer
nocte if hypotension) for reducing proteinuria
**IV Lasix, not oral due to drug absorption may be affected by
edema of gut wall (large doses of intravenous diuretic for
refractory cases)
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General management of nephrotic syndrome
(cont’d)
Hypercoagulability (↑ hepatic synthesis of pro-coagulant factors,
↑ platelet aggregation, ↑ urinary losses of anti-coagulant
factors)
 Anticoagulate with warfarin for 3-6 months (or until albumin
>25g/L) if no contraindications.
 Target INR is 2-3
Infection
Hyperlipidemia (↑ cholesterol & triglycerides, thought to be due
to hepatic lipoprotein synthesis in response to low oncotic
pressure)
 Statins will be prescribed (dietary restriction is usually
insufficient)
 In some cases, lipidemia will spontaneously resolved upon
settlement of nephrotic syndrome
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 Immunoglobulin A Nephropathy
A型免疫球蛋白腎病 (IgAN)
• Most common primary glomerulonephritis in the
world
• IgA deposit in kidney for unknown reason, trigger
inflammation and kidney damage

Pathogenesis:
IgA mesangial deposition rate> IgA clearance
capacity and/or Deposited IgA resistant to
clearance
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Materials adopted from Dr CHOW Kai-ming / PWH
Classical presentation of IgAN

Microscopic
Macroscopic
hematuria (with or
hematuria
without proteinuria)

AKI
CKD

Nephrotic

Materials adopted from Dr CHOW Kai-ming / PWH

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 How to treat IgAN?
• No cure for the disease
• Remember tight blood pressure control (<125/85 mmHg)
• ACEI or ARB to control hypertension and reduce proteinuria,
both of which are modifiable risk factors for progressive disease
• Corticosteroid (1g methylprednisolone IV for 3 days, repeated 2
months and 4 months later, Oral prednisolone 0.5 mg/kg on alt
days for 6 months)
• Research (1): For higher grades of proteinuria, omega-3 fatty
acids found in fish oils (polyunsaturated) is an option for
reducing inflammation in IgA nephropathy;
• Research (2): test effectiveness of immunosuppressive agent
mycophenolate mofetil (MMF) in reducing protein in urine and
slowing the progression of kidney disease with IgAN
Materials adopted from Dr CHOW Kai-ming / PWH 53
 Possible mechanisms from
corticosteroid effect
• Reduce proliferative lesion during acute phase
of IgAN
• Anti-inflammatory and immunosuppressive
properties

Materials adopted from Dr CHOW Kai-ming / PWH 54

 Polycystic kidney disease
Inherited kidney diseases
S/S: Renal enlargement with cysts, abdominal pain,
± hematuria (hemorrhage into a cyst), ↑BP
Diagnostic tests: USG, CT, MRI, genetic testing
Treatment: no specific treatment
Treat ↑BP and prevent infection
Complications: renal failure,
cardiovascular complications

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 Renal Tract Cancer
• Renal carcinoma • Renal tract carcinoma
- Fever - Pain
- Weight loss - Mass
- Malaise - Hematuria
- Neuropathy - Obstruction
- Myopathy
- Hormone production

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 Acute Kidney Injury (AKI)
Introduced by the Acute Kidney Injury Network (AKIN), specific
criteria exist for the diagnosis of AKI (previously called Acute
Renal Failure) :

 the abrupt (≤ 48 hours) reduction of kidney function

 Increased serum creatinine levels, absolute increase in
serum creatinine of ≥0.3 mg/dL (≥26.4 μmol/l) , percentage
increase in serum creatinine of ≥50%
OR
 Reduction in urine output, defined as <0.5 ml/kg/hr for more
than 6 hours
Mehta, R.L. et al, 2007
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Vrtis, 2013
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 Pathophysiology of AKI

↓ renal perfusion results in renin/angiotensin

release and aldosterone release and decrease
blood supply to the nephron.

Reduced blood flow decreases glomerular

pressure, GFR, and tubular flow; thus oliguria
occurs.

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Lameire et al, 2005 60
Walden, Ellis & Hicks, 2012

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 Major Causes of AKI
 Pre-renal failure (reduced renal perfusion)
1. Hypovolemia: hemorrhage, diarrhea, vomiting, reduced
effective circulating volume,i.e. severe heart failure, septic
shock, cirrhosis
2. Drugs: COX-2 inhibitors & NSAIDs (impair renal autoregulatory
responses by blocking the production of prostaglandin, which is
necessary to maintain renal perfusion)
ACEI: used to preserve and maintain renal fx in pts with DM, HT
& heart failure. But if the pt is already in AKI, these drugs can
worsen the situation
3. Renal artery stenosis
 Intra-renal failure
1. Tubular (obstruction & dysfunction): acute tubular necrosis
2. Glomerular: glomerulonephritis
3. Tubulointerstitial: drugs, myeloma, sarcoid
 Post-renal failure
1. Urinary tract obstruction (ureteric, bladder or urethra etc.)
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Murphy & Byrne, 2010

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Murphy & Byrne, 2010

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Mechanisms of Acute Tubular Necrosis
(Fry & Farrington, 2005)

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66
 Distinguishing pre-renal failure & ATN
Pre-renal ATN
Urine Na (mmol/L) <20 >40
Urine osmolarity (mosm/L) >500 <350
Urine / plasma urea >8 <3
Urine-plasma creatinine >40 <20
ratio
Fractional Na excretion (%) <1 >2

Longmore et al., 2007

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Murphy & Byrne, 2010

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 Four phases of AKI
1. The initiation phase
• The time between the kidney injury & the
reduction in kidney function
2. The oliguric phase
• The reduction of urine output (U/O) to 400 mL
in 24 hours, usually within 1 to 7 days after
the kidney injury and lasts 10 to 14 days (or
may lasts for weeks or months)

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 Findings in oliguric phase
Hyponatremia
Impaired renal absorption of Na and dilutional
hyponatremia
BUN & creatinine level ↑
Reflecting nitrogenous waste accumulation
Hyperkalemia
Metabolic acidosis
Fluid volume overload
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 Four phases of AKI (cont’d)
3. The diuretic phase (may last from 1 to 3 weeks)
• Starts with a U/O of 1 to 3 L per day, sometimes
increasing to 3 to 5 L or more per day.
• The nephrons have regained the ability to secrete urea,
which draws the fluid across the glomerular membrane
(osmotic diuresis). However, they don’t have the ability
to concentrate that flitrate.
• The kidneys have acquired their ability to excrete waste
but NOT concentrate urine.
• Must be monitored for hypotension, hypovolaemia,
continuing hyponatremia (due to sodium loss in the
flitrate) and hypokalemia 71
 Four phases of AKI (cont’d)
4. Recovery phase
• Filtration rates increases, allowing BUN and
serum creatinine levels to decrease and
electrolyte balance to be maintained
• Usually takes several weeks, but in some
cases, it continues for up to a year

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 The far-reaching effects of AKI
• Cardiovascular & pulmonary
- Fluid overloads results in HT, peripheral &
pulmonary edema
- Hyperkalemia causes arrhythmias
- Bradycardia, heart block & asystole could develop
if the serum potassium level rises above 6 mEq/L
• Fluids & electrolytes
- May lead to hyponatremia, hyperkalemia,
hyperphosphatemia and fluid overload

73
 The far-reaching effects of AKI (cont’d)
• Neurologic
- Metabolic wastes in the blood can cause sensory
changes, decreased mentation, confusion and coma
• Hematologic
- Anaemia (decreased erythropoietin production)
• Gastrointestinal
- Uremia causes loss of appetite, nausea, vomiting and
eventually a decrease in body mass and muscle
- Urea can cause a metallic taste in the mouth or a foul
urine odor to the breath
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Management of Kidney Injury

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 Stepwise Approach to Management
1. History of any urological & systemic symptoms, underlying
renal problem, and exposure to nephrotoxic agents.
2. Review of vital signs, fluid balance and medication.
3. Exam for hemodynamic and hydration status and features
of fluid overload.
4. Stop any nephrotoxic drug, i.e. NSAID
5. Insert a Foley catheter to monitor urine output.
6. Perform various blood tests and urine testing.
7. Monitor CVP may be needed, the aim is to maintain
adequate hydration and peripheral perfusion but avoid
iatrogenic fluid overload.
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 Clinical Assessment & Investigations(1)
Lab (Blood) Findings
• Hb • Decreased
• K • Increased
• Calcium • Decreased (cause tingling
of extremities)
• Plasma osmolality • Usually increased
• Plasma creatinine • Increased
• Na • Decreased (cause
twitching or seizures)

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 Clinical Assessment & Investigations(2)

Lab (Urine) Findings

• Specific gravity • Decreased (fixed in CKD)
• Urinary sediments • Normal to increased
• Urine osmolality • Decreased
• Sodium concentration • Decreased in Pre-renal but
will increase in ATN
(Intrinsic)
• Creatinine clearance
(GFR) • Decreased

78
 Clinical Assessment & Investigations(3)

Fluid Findings
• Urinary output • Decreased (less than
400mL/day or 30mL/hr, i.e.
insufficient to excrete
waste products)
• Skin turgor • Variable
• Edema • Usually present (need
dialysis)

79
O’Callaghan, 2009
80
Be cautious of nephrotoxic drugs

O’Callaghan, 2009

81
 Clinical Assessment & Investigations(4)
 Radiological tests:
1. Renal USG
2. Intravenous Pyelogram (IVP) – X-ray examination of
the kidneys, ureters and urinary bladder
3. Renal angiographies / renal scan
4. CT scan / MRI
 Other investigations
 Renal biopsy
 ECG, i.e. signs of hyperkalemia?
 CXR, i.e. any pulmonary edema?

82
 Management of AKI
1. Hyperkalemia: further explained on next slide
2. Pulmonary edema: Furosemide 250mg in 50 ml 0.9%
NS over 1 hr, high flow of oxygen
3. Metabolic Acidosis: 8.4% NaHCO3
4. Fluid balance: strict I&O
5. Dopamine: 1-3 μg/kg/min Dopamine (low dose) will
increase renal perfusion in critically ill patients
6. Diuretics: convert oliguric to non-oliguric AKI which
may help with fluid & electrolyte management
7. Relief of obstruction

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 Metabolic acidosis
• Common sign of AKI because hydrogen ion
secretion is impaired
• ABG shows a low pH and low bicarbonate
• Bicarbonate is low because it’s used to buffer the
elevated hydrogen ions
• May present Kussmaul respirations (rapid & deep
breaths), which is the body’s attempt to restore
the acid-base balance by removing more carbon
dioxide from the system (PaO₂ will be low)
• Severe acidosis hypotension, bradycardia,
alternation in level of consciousness 84
 Management of Hyperkalaemia
For urgent cases (serum K > 6mM &/or ECG changes of
hyper K) medical emergency because of the risk of
life threatening cardiac arrhythmias.
1. 10% Calcium gluconate :10mL IV over 2-3 minutes
with cardiac monitoring; repeat if no effect in 5
minutes (onset: 1-3 min; duration 30-60 min). If
digoxin toxicity is suspected, omit calcium gluconate
infusion.
2. Dextrose-insulin infusion: give 250mL D10 or 50 mL
D50 with 8-10 units Actrapid HM over 30 minutes;
repeat every 4-6 hrs if necessary (onset: 5-10 minutes;
duration: 4-6 hrs). Hospital Authority, 2011 85
 Management of Hyperkalaemia (cont’d)
3. Sodium bicarbonate 8.4% :100-150mL over 30-60 min;
to be given after calcium infusion in separate IV line;
watch out for fluid overload. (It fails to lower the
serum K+, only in life-threatening arrhythmias or
neuromuscular symptoms with metabolic acidosis.)
4. Resonium C/A: 15-50 g orally Q4-6 hrs or as retention
enema; may be given in 100-200mL 10% mannitol as
laxative; one gm resonium will bind 1 mmole of K.
5. Diuretics: Furosemide 40-80 mg IV bolus (remove K+
from the kidney)
6. Emergency haemodialysis or peritoneal dialysis
86
 Why use Dextrose / Insulin drip &
Ca gluconate as the initial treatment?
 Dextrose / Insulin (DI drip)
- Shift K+ from the blood into cell
 Calcium gluconate
- Protect the cardiac membrane
- It will NOT lower K+, but if ECG changes are present,
there should be improvement in ECG pattern within 1 to
3 minutes.
both treatments are temporary measure “buying time”
while measures are started to reduce the serum potassium
through increasing cellular uptake
87
For chronic cases of hyperkalaemia
Low K diet : < 2 g/day
Diuretics: Frusemide or Thiazide
Correct acidosis: Oral NaHCO3 300-900mg tds
(~10-30 mmol/day)
Fludrocortisone 0.1-0.2 mg daily
Long-term resonium therapy is poorly tolerated

88
Indications of renal replacement therapy
Severe hyperkalemia, unresponsive to medical therapy
Fluid overload with pulmonary edema
Uremia (blood urea > 30-50 mmol/l)
Complications of severe uremia: encephalopathy,
pericarditis, neuropathy / myopathy
Severe acidosis (pH < 7.1)
Drug overdose with a dialysable toxin

89
 Chronic Kidney Disease (CKD)
Definition:
It is a usually progressive and irreversible
deterioration, is the end result of gradual tissue
destruction and loss of kidney function.

When reaching end-stage renal failure (ESRF), a patient

will need some form of dialysis treatment or a kidney
transplant to survive, otherwise may die.

90
 National Kidney Foundation (NKF)
definition of CKD
• Kidney damage for 3 months or more, as defined by
structural or functional abnormalities of the kidney
with or without decreased GFR, manifested by
pathological abnormalities or markers of kidney
damage, including abnormalities in the composition
of the blood or urine or abnormalities in imaging
tests
• GFR<60 ml per minute per 1.73 m2 for 3 months or
more, with or without kidney damage

91
 Update on Definition and Staging of CKD

• Staging depends on the level of kidney function (i.e.

Glomerular filtration rate/ GFR)
• 24-hour urine collection of creatinine clearance was
formerly used as the marker of kidney function,
which is tedious and cumbersome for patients.
• Now with the help of computer, scientific formula
such as creatinine, age and gender is used to
estimate the GFR, where patients are then grouped
under different stages according to their estimated
GFR.
92
 National Kidney Foundation Classification of CKD
Stage Description Other terms GFR
used (ml/min/1.73 m2)

1 Kidney damage with At risk > 90

normal glomerular
filtration rate (GFR)

2 Kidney damage with Chronic renal 60 – 89

mild decrease in GFR insufficiency
(CRI)

3 Moderate decrease in CRI, chronic 30 – 59

GFR renal failure
(CRF)

4 Severe decrease in CRF 15 – 29

GFR

5 Kidney failure End-stage renal < 15

disease (ESRD)
93
 What are the causes of CKD?
The causes of new cases of end stage renal failure in Hong
Kong (2008) are:
1. DM – over 40%
2. Unknown reason - 20%
3. Glomerulonephritis - 19%
4. Hypertension / kidney vascular disease - 9%
5. Kidney stones / urinary obstruction – 3%
6. Genetic (polycystic kidney) – 4%
7. Urinary tract infection – 1%
(HAHO, 2010)

94
 Diabetic Nephropathy (DMN)
Definition
- Structural and function changes in kidney
related to DM
- Functional: hyperfiltration and proteinuria,
impaired renal function of various severity
- Structural: glomerulopathy with glomerular
basement membrane thickening, mesangial
expansion, nodular and then global
glomerulosclerosis
Materials adapted from Dr LO Kin-Yee, Associate Consultant of KWH 95
O’Callaghan, 2009
96
 Antidiabetic drug treatment in CKD
• Biguanides: Metformin can be used in patient
with mild to moderate CKD, avoid use if eGFR
<45ml/min/1.73m2 or serum creatinine
>132μmol/L in men and 123μmol/L in women
• Sulfonylureas: Tolbutamide & Glipizide are the
choices for CKD stage 3-5 as they are mainly
metabolized in liver
• Meglitinides: repaglinide (Prandin) is
principally metabolized in liver. Tends to use
lower dose in severe renal impairment
97
 Antidiabetic drug treatment in CKD
(cont’d)
• Thiazolidinediones or Glitazones: avoid
rosiglitazone (Avandia) because of increased
in cardiovascular mortality
• Dipeptidyl Peptidase-4 (DPP4) inhibitors:
reduce dose for sitagliptin (Januvia) if GFR <
50ml/min

Materials adapted from Dr LO Kin-Yee, Associate Consultant of KWH

98
 Preserving kidney function through
blood pressure control
• HT and DM are commonly associated
• High BP is a key pathogenic factor contributes
to renal deterioration (glomerular
hyperperfusion and hyperfiltration)
• Concrete evidences from many randomized
clinical trials showed that appropriate BP
control will delay the development and
progression of DMN or cardiovascular
complications
99
 Preserving kidney function through
BP control (cont’d)
• Most of current guidelines recommend BP goal
of 130/80 for DM patients, irrespective of the
presence of CKD
• There is concern of lower diastolic BP
(<75mmHg) may impair myocardial perfusion.
BP lowering should be less aggressive in
patients with preexisting cardiovascular
problems
• A single target BP does not fit all DM patients
Materials adopted from Dr LO Kin-Yee, Associate Consultant of KWH 100
 How to delay renal deterioration ?
Control BP and DM
 Diet control
 Anti-hypertensive drugs
 Hypoglycemic drugs
 Reducing body weight
Drug compliance
 Calcium & Iron supplement
 Phosphate binder
 Avoid Chinese herbs
Diet compliance
 Avoid star fruit
 Low protein
 Low potassium
 Low phosphate
 Low salt
 Fluid restriction
101
 Common medications of CKD
 To control high blood pressure
 ACEI or ARB, combination with Ca blocker
 To lower cholesterol
 Zocor, Lipitor
 DM control
 Tolbutamide and insulin SC injection
 To relieve anemia
 Folate, Vitamin B6, Iron supplement or Human recombinant
erythropoietin 4000-5000 unit SC/IV weekly

102
 Common medications of CKD (cont’d)
 To relieve swelling
 Furosemide 250mg-2g/daily or metolazone 5-10mg/daily if
patient has urine output
 Medications to protect your bones
 PO4 binder: Calcium carbonate 1.5-3.0 g bd or tds with meal,
Aluminium Hydroxide 0.6-1.2 g bd or tds
 Vitamin D: Alfacalcidol or Calcitriol 0.25-1.0 ug OM , 2-3 times
per week
 Dermatology treatment (for pruritus because of ammonia which
can progress to uremic frost on skin)
 Atarax; Phenergan; Eurax Cream

103
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