OPEN UNIVERSITY OF MALAYSIA RENAL NURSING – NBNS3504 Dr. S. Nishan Silva (MBBS)

OPEN UNIVERSITY OF MALAYSIARENAL NURSING – NBNS3504

Dr. S. Nishan Silva(MBBS)

FUNCTIONS OF THE URINARY SYSTEM

Elimination of waste productsNitrogenous wastes e.g. urea, uric acid, creatinine

ToxinsDrugs

FUNCTIONS OF THE URINARY SYSTEM

Regulate aspects of homeostasisWater balanceElectrolytesAcid-base balance in the blood (pH)Blood pressureRed blood cell productionActivation of vitamin D

ORGANS OF THE URINARY SYSTEM

Figure 15.1a

Kidneys

Ureters

Urinary bladder

Urethra

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Transverse sections show retroperitoneal position of kidneys

Note also: liver, aorta muscles on CT

Note layers of adipose (fat), capsule, fascia

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FOR STUDYING

Parts of the kidney:1. Renal pyramid2. Efferent vessel3. Renal artery4. Renal vein5. Renal hilum6. Renal pelvis7. Ureter8. Minor calyx9. Renal capsule10. Inferior renal capsule11. Superior renal capsule12. Afferent vessel13. Nephron14. Minor calyx15. Major calyx16. Renal papilla17. Renal column

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Kidney has two regionsCortex: outer

Columns of cortex divide medulla into “pyramids”Medulla: inner

Darker, cone-shaped medullary or renal pyramids Parallel bundles of urine-collecting tubules

LOCATION OF THE KIDNEYS

At the level of T12 to L3

Attached to ureters, renal blood vessels, and nerves at renal hilus

On top of each kidney is an adrenal gland

REGIONS OF THE KIDNEY

Figure 15.2b

Renal cortex – outer region

Renal medulla – inside the cortex

Renal pelvis – inner collecting tube

KIDNEY STRUCTURES

Medullary pyramids – triangular regions of tissue in the medulla

Renal columns – extensions of cortex-like material inward

Calyces – cup-shaped structures that funnel urine towards the renal pelvis

NEPHRONS

Main structures of the nephrons

Glomerulus Renal tubule

GLOMERULUS

A specialized capillary bed

Attached to arterioles on both sides (maintains high pressure)

Large afferent arteriole

Narrow efferent arteriole

Figure 15.3c

BLOOD FLOW IN THE KIDNEYS

Figure 15.2c

GLOMERULUS

Capillaries are covered with podocytes from the renal tubule

The glomerulus sits within a glomerular capsule (the first part of the renal tubule)

Figure 15.3c

RENAL TUBULE

Glomerular (Bowman’s) capsule

Proximal convoluted tubule

Loop of HenleDescending limbAscending limbDistal

convoluted tubule

Straight collecting tubule

Figure 15.3b

PERITUBULAR CAPILLARIES

Arise from efferent arteriole of the glomerulus

Normal, low pressure capillaries

Attached to a venule

Cling close to the renal tubule

Reabsorb (reclaim) some substances from collecting tubes

URINE FORMATION PROCESSES

Filtration

Reabsorption

Secretion

Figure 15.4

FILTRATION

Nonselective passive process

Water and solutes smaller than proteins are forced through capillary walls

Blood cells cannot pass out to the capillaries

Filtrate is collected in the glomerular capsule and leaves via the renal tubule

REABSORPTION

Some reabsorption is passive, most is active

Most reabsorption occurs in the proximal convoluted tubule

SECRETION – REABSORPTION IN REVERSE

Some materials move from the peritubular capillaries into the renal tubules

Hydrogen and potassium ionsCreatinine, ureaPenicillin, cocaine, marijuana, many food preservatives, and some pesticides

FORMATION OF URINE

Figure 15.5

CHARACTERISTICS OF URINE USED FOR MEDICAL DIAGNOSIS

Colored somewhat yellow due to the pigment urochrome (from the destruction of hemoglobin) and solutes

Clear

Sterile

Slightly aromatic

Normal pH of around 6

Specific gravity of 1.001 to 1.035

URETERS

Continuous with the renal pelvis

Enter the posterior aspect of the bladder

Run behind the peritoneum

Peristalsis (they contain smooth muscle) aids gravity in urine transport

URINARY BLADDER

Figure 15.6

Smooth, collapsible, muscular sac

Temporarily stores urine

URINARY BLADDER

Trigone – three openingsTwo from the uretersOne to the urethrea

Figure 15.6

URINARY BLADDER WALL

Composed of three layers:Outer layer – loose connective tissue covered on the upper surface by the peritoneum

Middle layer - three layers of smooth muscle (detrusor muscle)

Inner layer - mucosa made of transitional epithelium

Walls are thick and folded in an empty bladder, can expand significantly without increasing internal pressure

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THE URETHRASmooth muscle with inner mucosa Changes from transitional through stages to stratified squamous near

end Drains urine out of the bladder and body

Male: about 20 cm (8”) longFemale: 3-4 cm (1.5”) long Short length is why females have more urinary tract infections than

males - ascending bacteria from stool contamination

Urethra____

urethra

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Urethral sphincters Internal: involuntary sphincter of smooth muscleExternal: skeletal muscle inhibits urination voluntarily until proper time (levator anni muscle also helps voluntary constriction)

Males: urethra has three regions (see right)

1. Prostatic urethra__________

2. Membranous urethra____

3. Spongy or penile urethra_____

_________trigone

female

URETHRA

Release of urine is controlled by two sphincters

Internal urethral sphincter (involuntary)External urethral sphincter (voluntary)

URETHRA GENDER DIFFERENCES

LocationFemales – along wall of the vagina and opens to the outside at the urethral meatus between the labia minora.

Males – through the prostate and penis

FunctionFemales – only carries urineMales – carries urine and is a passageway for sperm cells

STORAGE REFLEXES

MICTURITION REFLEXES

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Micturition AKA:

Voiding Urinating Emptying the bladder

(See book for diagramexplanation p 701)

KNOW:Micturition center of brain:

pons(but heavily influenced by

higher centers) Parasympathetic: to voidSympathetic: inhibits

micturition

URINE

ANALYSIS

COLLECTION OF URINE

Early morning sample-qualitative

Random sample- routine24hrs sample- quantitativeMidstream sample-UTIPost prandial sample-D.M

Clean Catch

Specimen Collection

Supra-pubic Needle Aspiration

24 HOUR URINE SAMPLE

1. For quantitative estimation of proteins

2. For estimation of vanillyl mandelic acid, 5-hydroxyindole acetic acid, metanephrines

3. For detection of AFB in urine

4. For detection of microalbuminuria

URINARY VOLUME

Normal = 600-1550ml

Polyuria- >2000ml

Oliguria-<400ml

Anuria-complete cessation of urine(<200ml)

Nocturia-excretion of urine by a adult of >500ml with a specific gravity of <1.018 at night (characteristic of chronic glomerulonephritis)

COLOR & APPEARANCE

Normal= clear & pale yellow

1. Colourless- dilution, diabetes mellitus, diabetes insipidus, diuretics

2. Milky-purulent genitourinary tract infection, chyluria

3. Orange-fever, excessive sweating

4. Red-beetroot ingestion,haematuria

5. Brown/ black- alkaptunuria, melanin

URINARY PH/ REACTION

Reaction reflects ability of kidney to maintain normal hydrogen ion concentration in plasma & ECF

Normal= 4.6-8

Tested by- 1.litmus paper

2. pH paper

3. dipsticks

ODOUR

Normal= aromatic due to the volatile fatty acids

Ammonical – bacterial action

Fruity- ketonuria

SPECIFIC GRAVITY

Depends on the concentration of various solutes in the urine.

Measured by-urinometer

- refractometer

- dipsticks

URINOMETER

Take 2/3 of urinometer container with urine

Allow the urinometer to float into the urine

Read the graduation at the lowest level of urinary meniscus

Correction of temperature & albumin is a must.

Urinometer is calibrated at 15or 200cSo for every 3oc increase/decrease

add/subtract 0.001For 1gm/dl of albumin add0.001

CHEMICAL EXAMINATION

ProteinsSugarsKetone bodiesBilirubinBile saltsUrobilinogenBlood

MICROSCOPIC EXAMINATION

Microscopic urinalysis is done simply pouring the urine sample into a test tube and centrifuging it (spinning it down in a machine) for a few minutes. The top liquid part (the supernatant) is discarded. The solid part left in the bottom of the test tube (the urine sediment) is mixed with the remaining drop of urine in the test tube and one drop is analyzed under a microscope

CRYSTALS IN URINE

Crystals in acidic urine

Uric acid

Calcium oxalate

Cystine

Leucine

Crystals in alkaline urine

Ammonium magnesium phosphates(triple phosphate crystals)

Calcium carbonate

CRYSTALS

CASTS

Urinary casts are cylindrical aggregations of particles that form in the distal nephron, dislodge, and pass into the urine. In urinalysis they indicate kidney disease. They form via precipitation of Tamm-Horsfall mucoprotein which is secreted by renal tubule cells.

TYPES OF CASTS

Acellular casts

Hyaline casts

Granular casts

Waxy casts

Fatty casts

Pigment casts

Crystal casts

Cellular casts

Red cell casts

White cell casts

Epithelial cell cast

GRANULAR CASTS

Granular casts can result either from the breakdown of cellular casts or the inclusion of aggregates of plasma proteins (e.g., albumin) or immunoglobulin light chains

indicative of chronic renal disease

Microscopic Examination Granular Cast

Microscopic Examination WBCs Cast

Microscopic Examination RBCs Cast -

Histology

Chemical AnalysisUrine

DipstickGlucoseGlucose

BilirubinBilirubin

KetonesKetones

Specific GravitySpecific Gravity

BloodBlood

pHpH

ProteinProtein

UrobilinogenUrobilinogen

NitriteNitrite

Leukocyte EsteraseLeukocyte Esterase

BLOOD ANALYSIS

(Of creatinine)

Glomerulofiltration Rate

ESTIMATED GFR

GFR Calculatorhttp://easycalculation.com/medical/gfr.php

RENAL SCAN

RENAL ARTERIOGRAM

INTRAVENOUS PYELOGRAM

RENAL BIOPSY

PYELO

NEPHRIT

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S

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ETIOLOGY❏ usually ascending microorganisms, most often

bacteria

❏ in females with uncomplicated pyelonephritis usually E. coli

❏ causative microorganisms are usually E. coli, Klebsiella, Proteus, Serratia, Pseudomonas, Enterococcus, and S. aureus

❏ if S. aureus is found, suspect bacteremic spread from a distant focus (e.g. septic emboli in infective endocarditis) and suspect (possible multiple intra-renal microabscesses or perinephric abscess)

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CLINICAL PRESENTATION

❏ rapid onset (hours to a day)

❏ lethargic and unwell, fever, tachycardia, shaking, chills, nausea and vomiting, myalgias

❏ marked CVA or flank tenderness; possible abdominal pain on deep palpation

❏ symptoms of lower UTI may be absent (urgency, frequency, dysuria)

❏ may have symptoms of Gram negative sepsis

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INVESTIGATIONS

❏ urine dipstick: +ve for leukocytes and nitrites, possible hematuria

❏ microscopy: > 5 WBC/HPF in unspun urine or > 10 WBC/HPF in spun urine, bacteria

❏ Gram stain: Gram negative rods, Gram positive cocci

❏ culture: > 105 colony forming units (CFU)/mL in clean catch midstream urine or > 102 CFU/mL in suprapubic aspirate or catheterized specimen

❏ CBC and differential: leukocytosis, high % neutrophils

❏ blood cultures: may be positive in 20% of cases, especially in S. aureus infection

❏ consider investigation of complicated pyelonephritis: if fever, pain, leukocytosis not resolving with treatment within 72 hr, if male patient, or if there is history of urinary tract abnormalities (abdo /pelvis U/S, CT for renal abscess, spiral CT for stones, cystoscopy)

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COMPLICATIONS

Chronicity

Bacteraemia or Septicaemia

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TREATMENT❏ uncomplicated pyelonephritis with mild

symptoms

• 14 day course of TMP/SMX (trimethoprim-sulfamethoxazole) or fluoroquinolone or third generation cephalosporin

• start with IV for several days and then switch to PO (can then be treated as outpatient)

❏ patient more than mildly symptomatic or complicated pyelonephritis in the setting of stone obstruction is an urologic emergency (placing patient at risk of kidney loss or septic shock)

• start broad spectrum IV antibiotics until cultures return (imipenem or emropenem or piperacillin /tazobactam or ampicillin+gentamicin) and treat 2-3 weeks

• follow-up cultures 2-4 weeks after stopping treatment

❏ if no improvement in 48-72 hr, need to continue on IV antibiotics, assess for complicated pyelonephritis or possible renal or perinephric abscess

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GLOMERULONEPHRITIS

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Electron micrograph of a normal glomerular capillary loop showing the fenestrated endothelial cell (Endo), the glomerular basement membrane (GBM), and the epithelial cells with its interdigitating foot processes (arrow). The GBM is thin and no electron dense deposits are present. Two normal platelets are seen in

the capillary lumen. Courtesy of Helmut Rennke, MD.

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Capillary Space

Endothelium

Urinary Space

GBM

Podocyte

FILTRATION MEMBRANE – ELECTRON MICRO.

MD consult

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Electron micrograph in dense deposit disease (DDD) showing dense, ribbon-like appearance of subendothelial and intramembranous material (arrow) and narrowing of the capillary lumen due to proliferation of cells (double arrow). Courtesy of Helmut Rennke, MD.

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POSSIBLE CLINICAL MANIFESTATIONS

Proteinuria – asymptomatic

Haematuria – asymptomatic

Hypertension

Nephrotic syndrome

Nephritic syndrome

Acute renal failure

Rapidly progressive renal failure

End stage renal failure

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DIAGNOSIS

Look for clues History

Haematuria Proteinuria Azotemia azote – nitrogen A – without Zoe – life “The gas does not support life” (French chemists Gayton de Morveau

(1737-1816) and Antoine Lavoisier (1743-1794) )

McCarthy ET, November 2008

NEPHROTIC SYNDROME

Nephrotic syndrome (NS) results from increased permeability of Glomeulrar basement membrane (GBM) to plasma protein.

It is clinical and laboratory syndrome characterized by massive proteinuria, which lead to hypoproteinemia ( hypo-albuminemia), hyperlipidemia and pitting edema.

(4-increase, 1-decrease).

NEPHROTIC CRITERIA:-

*Massive proteinuria: qualitative proteinuria: 3+ or 4+, quantitative proteinuria : more than 40 mg/m2/hr in children (selective).

*Hypo-proteinemia : total plasma proteins < 5.5g/dl and serum albumin : < 2.5g/dl.

*Hyperlipidemia: serum cholesterol : > 5.7mmol/L

*Edema: pitting edema in different degree

NEPHRITIC CRITERIA

-Hematuria: RBC in urine (gross hematuria)

-Hypertension: ≥130/90 mmHg in school-age children ≥120/80 mmHg in preschool-age children ≥110/70 mmHg in infant and toddler’s children

-Azotemia （ renal insufficiency ） : Increased level of serum BUN 、 Cr-Hypo-complementemia: Decreased level of serum c3

Oliguria, Oedema, Albuminurea

CLASSIFICATION:

A-Primary Idiopathic NS (INS): majority

The cause is still unclear up to now. Recent 10 years ,increasing evidence has suggested that INS may result from a primary disorder of T– cell function.

Accounting for 90% of NS in child. mainly discussed.

B-Secondary NS:

NS resulted from systemic diseases, such as anaphylactoid purpura , systemic lupus erythematosus, HBV infection.

C-Congenital NS: rare

*1st 3monthe of life ,only treatment renal transplantation

SECONDARY NS Drug,Toxic,Allegy: mercury, snake venom, vaccine, pellicillamine,

Heroin, gold, NSAID, captopril, probenecid, volatile hydrocarbons

Infection: APSGN, HBV, HIV, shunt nephropathy, reflux nephropathy, leprosy, syphilis, Schistosomiasis, hydatid disease

Autoimmune or collagen-vascular diseases: SLE, Hashimoto’s thyroiditis,, HSP, Vasculitis

Metabolic disease: Diabetes mellitus

Neoplasma: Hodgkin’s disease, carcinoma ( renal cell, lung, neuroblastoma, breast, and etc)

Genetic Disease: Alport syn, Sickle cell disease, Amyloidosis, Congenital nephropathy

Others: Chronic transplant rejection, congenital nephrosclerosis

IDIOPATHIC NS (INS): PATHOLOGY:-

Minimal Change Nephropathy (MCN): <80%The glomeruli appear normal basically Under

Light microscopy, and Under Immunofluorescence

*under Electron microscopy – fusion of the foot processes of the podocytes

(2) Non—MCN ： ＜ 20%*Mesangial proliferative glomerulonephritis

(MsPGN): about 10%*Focal segmental glomerulosclerosis (FSGS): 5%*Membranous Nephropathy (MN) : 2% *Membrane proliferative glomerulonephritis

(MPGN) : 1% *Others ： rare,Cresent glomerulonephritis

CLINICAL MANIFESTATION:-

IN MCNS , The male preponderance of 2:1

: 1.Main manifestations:

Edema (varying degrees) is the common symptomLocal edema: edema in face , around eyes( Periorbital swelling) , in

lower extremities. Generalized edema (anasarca), edema in penis and scrotum.

2-Non-specific symptoms:

Fatigue and lethargyloss of appetite, nausea and vomiting ,abdominal pain , diarrhea

body weight increase, urine output decrease pleural effusion (respiratory distress)

INVESTIGATIONS:-

1-Urine analysis:-

A-Proteinuria : 3-4 + SELECTIVE.

b-24 urine collection for protein>40mg/m2/hr for children

c- volume: oliguria (during stage of edema formation)

d-Microscopically:-

microscopic hematuria 20%, large number of hyaline cast

INVESTIGATIONS:-

2-Blood:A-serum protein: decrease >5.5gm/dL , Albumin levels are low ( ＜ 2.5gm/dL).

B-Serum cholesterol and triglycerides: Cholesterol ＞ 5.7mmol/L (220mg/dl).

C-- ESR↑ ＞ 100mm/hr during activity phase

.3.Serum complemen: Vary with clinical type.

4.Renal function

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KIDNEY BIOPSY:-

Considered in:

1-Secondary N.S

2-Frequent relapsing N.S

3-Steroid resistant N.S

4- Hematuria

5-Hypertension

6- Low GFR

COMPLICATIONS OF NS:-

1-Infections:Infections is a major complication in children with NS. It frequently trigger relapses.

Nephrotic pt are liable to infection because :A-loss of immunoglobins in urine.B-the edema fluid act as a culture medium.C-use immunosuppressive agents.

D- malnutrition

The common infection : URI, peritonitis, cellulitis and UTI may be seen.

Organisms: encapsulated (Pneumococci, H.influenzae), Gram negative (e.g E.coli

COMPLICATION …

Vaccines in NS;-

polyvalent pneumococcal vaccine (if not previously immunized) when the child is in remission and off daily prednisone therapy.

Children with a negative varicella titer should be given varicella vaccine.

COMPLICATION…..

2-Hypercoagulability (Thrombosis).

Hypercoagulability of the blood leading to venous or arterial thrombosis:

Hypercoagulability in Nephrotic syndrome caused by: 1-Higher concentration of I,II, V,VII,VIII,X and fibrinogen

2- Lower level of anticoagulant substance: antithrombin III

3-decrease fibrinolysis.

4-Higher blood viscosity

5- Increased platelet aggregation

6- Overaggressive diuresis

3-ARF: pre-renal and renal

4- cardiovascular disease :-Hyperlipidemia, may be a risk factor for cardiovascular disease.

5-Hypovolemic shock

6-Others: growth retardation, malnutrition, adrenal cortical insufficiency

GENERAL THERAPY:-

Hospitalization:- for initial work-up and evaluation of treatment.

Activity: usually no restriction , except

massive edema,heavy hypertension and infection.

Diet Hypertension and edema: Low salt diet (<2gNa/ day) only during period of edema or salt-free diet. Severe edema: Restricting fluid intake

Avoiding infection: very important.

Diuresis: Hydrochlorothiazide (HCT) ： 2mg/kg.d

Antisterone ： 2 ～ 4mg/kg.d

Dextran ： 10 ～ 15ml/kg , after 30 ～ 60m,

followed by Furosemide (Lasix) at 2mg/kg .

INDUCTION USE OF ALBUMIN:-

Albumin + Lasix (20 % salt poor)

1-Severe edema

2-Ascites

3-Pleural effusion

4-Genital edema

5-Low serum albumin

CORTICOSTEROID—PREDNISONE THERAPY:-

Prednisone tablets at a dose of 60 mg/m2/day (maximum daily dose, 80 mg divided into 2-3 doses) for at least 4 consecutive weeks.

After complete absence of proteinuria, prednisone dose should be tapered to 40 mg/m2/day given every other day as a single morning dose.

The alternate-day dose is then slowly tapered and discontinued over the next 2-3 mo.

TREATMENT OF RELAPSE IN NS:

Many children with nephrotic syndrome will experience at least 1 relapse (3-4+proteinuria plus edema).

daily divided-dose prednisone at the doses noted earlier (where he has the relapse) until the child enters remission (urine trace or negative for protein for 3 consecutive days).

The pred-nisone dose is then changed to alternate-day dosing and tapered over 1-2 mo.

ACCORDING TO RESPONSE TO PREDNISONE THERAPY:

*Remission: no edema, urine is protein free for 5 consecutive days.

* Relapse: edema, or first morning urine sample contains > 2 + protein for 7 consecutive days.

*Frequent relapsing: > 2 relapses within 6 months (> 4/year).

*Steroid resistant: failure to achieve remission with prednisolone given daily for 28 days.

ALTERNATIVE AGENT:-

When can be used:

Steroid-dependent patients, frequent relapsers, and steroid-resistant patients.

Cyclophosphamide Pulse steroids

Cyclosporin A

Tacrolimus

Microphenolate

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Diseases PSGN IgA Nephropathy MPGN RPGN

Age and Sex All ages, mean 7 years, 2:1 male

2:1 male, 15-35 yrs 6:1 male, 15-30 yrs Mean 51yrs, 2:1 male

Clinical Manifestations 90% 50% 90% 90%

Acute nephritic syndrome

Occasionally 50% Rare rare

Asymptomatic haematuria

10-20% Rare Rare 10-20%

Nephrotic syndrome 70% 30-50% Rare 25%

Hypertension 50% Rare 50% 60%

Acute renal failure Latent 1-3 weeks Follows viral infection Pul haemorrhage, iron def

none

Lab findings ASOT IgA +anti GBM membrane + ANCA

Positive streptozyme IgA in dermal caps

C3-C9 N C1 and C4

Immunogenetics HLA B12

Light microscopy Diffuse proliferation Focal proliferation Focal- diffuse crescentic Crescentic GN

Immunoflourescence Granular IgG and C3 Diffuse mesangial IgA Linear IgG and C3 No immune complexes

Electron microscopy Subepithelial humps Mesangial deposits No deposits No deposits

Prognosis 95% cure5% progress

Slow progression in 25-50 years

75% stabilise or improve if treated early

75% stabilise or improve if treated early

Treatment Supportive None established Plasman exchange, cyclosphosphamide, steroids

Pulsed steroid therpy