Professional Documents
Culture Documents
NT Week 9
NT Week 9
NT Week 9
NT4_2017-18
1
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
2
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
3
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)
4
Ali & Gray-Vickrey, 2011
9
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.
10
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.
11
12
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
15
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
16
Renal & urological assessment (3)
Past health history
Childhood and infectious diseases
Trauma
Major illnesses and Hospitalizations
Operations
Medications
Allergies
17
Renal & urological assessment (4)
18
Diagnostic investigations
19
Renal biopsy
Three reasons
1. Establish the exact diagnosis
2. Determine therapy
3. Prognosis: degree of active (potentially
reversible) and chronic (Irreversible) changes
24
Parts of urinary tract affected Signs & symptoms
25
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
27
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
32
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)
33
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.
35
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).
36
Percutaneous nephrolithotomy (PCNL)
Prevention of renal calculi
37
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
38
39
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
40
5 Clinical syndromes of glomerular disease
O’Callaghan, 2009
43
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
45
Pathophysiology of Nephrotic Syndrome
↑ in glomerular permeability
Loss of Ig / complement
Loss of anticoagulant Loss of albumin
↓ albumin Infection
↑ tubular
Thromboemoblism absorption
↑ lipoprotein
Tubular synthesis
dysfunction Edema
Hyperlipidemia
Pathogenesis:
IgA mesangial deposition rate> IgA clearance
capacity and/or Deposited IgA resistant to
clearance
51
Materials adopted from Dr CHOW Kai-ming / PWH
Classical presentation of IgAN
Microscopic
Macroscopic
hematuria (with or
hematuria
without proteinuria)
AKI
CKD
Nephrotic
55
Renal Tract Cancer
• Renal carcinoma • Renal tract carcinoma
- Fever - Pain
- Weight loss - Mass
- Malaise - Hematuria
- Neuropathy - Obstruction
- Myopathy
- Hormone production
56
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) :
59
Lameire et al, 2005 60
Walden, Ellis & Hicks, 2012
61
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.)
62
Murphy & Byrne, 2010
63
Murphy & Byrne, 2010
64
Mechanisms of Acute Tubular Necrosis
(Fry & Farrington, 2005)
65
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
67
Murphy & Byrne, 2010
68
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)
69
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
70
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
72
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
74
Management of Kidney Injury
75
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.
76
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)
77
Clinical Assessment & Investigations(2)
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
83
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.
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
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
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 compliance
Diet control Avoid star fruit
Anti-hypertensive drugs Low protein
Hypoglycemic drugs Low potassium
Reducing body weight Low phosphate
Low salt
Drug compliance Fluid restriction
Calcium & Iron supplement
Phosphate binder
Avoid Chinese herbs
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
References
Ali, B., Gray-Vickrey, P. (2011). Limiting the damage from acute kidney injury. Nursing 2011, 41(3), 22-31.
Anatomy & physiology made incredibly easy. (2009). Philadelphia: Lippincott Williams & Wilkins.
Black, J.M., Hawks, J.H., Keene, A. & Luckmann, J. (2009). Medical-surgical nursing: Clinical management for positive
outcomes (8th ed.). Philadelphia: W.B. Saunders Company.
Bhalla et al. (2009). Melamine nephrotoxicity: An emerging epidemic in an era of globalization. Kidney International,
75(8), 774-779. Retrieved on 6 Oct 2010 from http://www.medscape.com/viewarticle/702630
Chu, P.S.K et al. (2007). ‘Street ketamine’ – associated bladder dysfunction: a report of ten cases. Hong Kong Med J,
13(4), 311- 313. Retrieved on 15 Aug 2010 from http://www.hkmj.org/article_pdfs/hkm0708p311.pdf
Diabetic nephropathy. (2010). U.S. National Library of Medicine. Retrieved on 17 Aug 2010 from
http://www.nlm.nih.gov/medlineplus/ency/article/000494.htm
Expert LPN guides: advanced skills. (2007). Philadelphia: Lippincott Williams & Wilkins.
Fry, A.C., Farrington. K., (2006). Management of acute renal failure. Post Graduate Medical Journal, 82(964), 106-116.
Retrieved on 15 Aug 2010 from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2596697/?tool=pubmed
Hospital Authority Head Office, COC(Med). (2011). Handbook of internal medicine (6th ed.).
Hospital Authority. (2010). Smart Patient. Retrieved on 16 August 2010 from 104
http://www21.ha.org.hk/smartpatient/en/home.html
References (cont’d)
Kontiokari, T., Sundqvist, K., Nuutinen, M., Pokka, T., Koskela, M., & Uhari, M. (2001). Randomised trial
of cranberry-lingonberry juice and Lactobacillus GG drink for the prevention of urinary tract
infections in women. BMJ,322:1-5.
Lai, K.N. (2009). A practical manual of renal medicine: nephrology, dialysis and transplantation.
Singapore: World Scientific
Lameire, N., Biesen, W.V. & Vanholder, R. (2005). Acute renal failure. Lancet, 365, 417-430.
Longmore, M., Wilkinson, I., Turmezei, T., Cheung C.K. (2007). Oxford handbook of clinical medicine
(7th ed.). New York: Oxford University Press.
Mehta, R.L., Kellum, J.A., Shah, S.V., Molitoris, B.A., Ronco, C., Warnock, D.G., Levin, A. & the Acute
Kidney Injury Network. (2007). Acute Kidney Injury Network: report of an initiative to improve
outcomes in acute kidney injury. Critical Care, 11(R31), 1-8.
O’Callaghan, C. (2009). The renal system at a glance (3rd ed.). Oxford: Wiley-Blackwell.
Paton, M. (2007). Acute renal failure. Nursing Made Incredibly Easy, 5(5), 29-38.
Pathophysiology made incredibly easy. (2009). Philadelphia: Lippincott Williams & Wilkins.
105
References (cont’d)
Steddon, S., Ashman, N., Chesser, A., Cunningham, J. (2006). Oxford handbook of nephrology and
hypertension (1st ed.). New York: Oxford University Press.
Vrtis, M.C. (2013). Preventing and responding to acute kidney injury. AJN, 113(4), 38-47.
Walden, P., Ellis, D., Hicks, R. (2012). Know the flow: kidney disease. Nursing Made Incredibly
Easy, 10(5), 18-28.
Ward, K. (2005). Kidneys, don’t fail me now! Nursing Made Incredibly Easy, 3(2), 18-27 .
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