Urinary system disorders

Seth Selassie Dzah

Department of Adult Health
University of Cape Coast
 The urinary system, is a
group of organs in the body
Definition that filters out excess fluid
and other substances from
the bloodstream.
 Eliminate wastes from the body
Regulate blood volume and
pressure
Control levels of electrolytes and
Functions metabolites
Regulate blood pH
Adrenal gland’s erythropoietin
productions contributes to RBCs
production
 A&P
review
Notice the difference
in length of urethra.

What is the potential

implication of that?
Nephron
 Notice close
association
between nephron
and blood vessels
Stages of
urine
formation
Notice differences
in size of afferent
and efferent
arteriole

What is the
implication?
 Forces
control
ultra
filtration
 Selective
reabsorption
explained

Que.: What does renal threshold mean?

  Needed because of the short ultra
filtration time
Tubular  H+ ions are secreted to control blood
secretion pH
explained
 Drugs such as aspirin, penicillin
excreted
 Urine 
composition
  Parathyroid hormone (↑blood Ca2+)
and calcitonin (↓blood Ca2+)
 ADH increased water reabsorption
Relevant  Aldosterone reabsorption of Na+ and
hormones water; excretion of potassium
 Atrial natriuretic peptide secreted by
atria decrease reabsorption of Na+ and
water
 New Glomerulonephritis
subtopic
 Encompasses a subset of renal
diseases
It is characterized by immune-
mediated damage to the glomerulus
Introduction 
Leads to hematuria, proteinuria, and
azotemia (elevated BUN & serum
creatinine)
Can be acute or chronic
Depiction
 o Acute
• primary renal cause
• secondary illness
acute post-Streptococcal
Aetiology glomerulonephritis streptococcal
infection
Staphylococcus aureus infection
oChronic due to progressing acute
leading to CKD and ESRD
 It is immune-mediated: both humoral and cell-
mediated pathways are active.
Results in inflammatory response leading to fibrotic
events that follow.
Subsequent events depend on underlying cause. E.g.
glomerulonephritis associated with staphylococcus
Pathophysiology shows IgA and C3 complement deposits
One of the targets is the glomerular basement
membrane itself or some antigen trapped within it,
as in post-streptococcal disease
Systemic antigen-antibody reactions with
glomerulonephritis occurring as one of the
components of the disease process, such as in
systemic lupus erythematosus (SLE)
 Proteinuria
Hematuria
Reduction in creatinine clearance, oliguria, or
anuria
Implications Active urine sediments, such as RBCs and
RBC casts
Intravascular volume expansion, edema, and
systemic hypertension.
 Specific symptoms
Hypertension
Clinical Edema initially in the dependent areas
manifestations Abnormal urinary sedimentation
Hematuria – microscopic or gross
Oliguria
 Azotemia
Dyspnea on exertion
Clinical Headache
manifestations
Confusion
Flank pain
 Nonspecific symptoms
generalized weakness
Clinical fever
manifestations
abdominal discomfort
malaise
 Related to underlying conditions:
Triad of sinusitis, pulmonary infiltrates,
and nephritis – granulomatosis with
polyangiitis
Clinical Nausea, vomiting, abdominal pain
manifestations Arthralgias - systemic lupus erythematosus
Hemoptysis - idiopathic progressive
glomerulonephritis
Skin rashes – in hypersensitivity vasculitis
 History
Physical examination
Lab investigations
oBlood
Diagnosis • Complete blood count
• Serum electrolytes
• Renal function tests
• Liver function tests
• C-reactive protein
 oUrine
•Microscopy
•Culture
Diagnosis •RBC casts
•Albumin to creatinine
oImaging i.e. renal ultrasound
oRenal biopsy
 Dietary modification
• Low salt
• Holding animal protein
Management • Restricting fluids
Edema
• Monitor intake and output
• Daily weighing
• Diuretics
 Monitoring vitals i.e. BP etc
Antihypertensives
• Loop diuretics (reduce edema and correct
HPT).
Management • ACE inhibitors
• Angiotensin 2 receptor blockers
Corticosteroids e. g. prednisolone
Analgesics
Balance activity and rest
 New Nephrotic syndrome
subtopic
 Inflammation of the glomeruli
leading to protein leakage from
the blood into the urine
(proteinuria).
Introduction
Results in low levels of
protein (albumin) in the blood
(hypoalbuminemia)
Depiction
 A group of symptoms indicating
impaired kidney function
Proteinuria
Hypoalbuminemia
Introduction
Edema
High levels of cholesterol and
other lipids (fats) in the blood
(hyperlipidemia)
 oPrimary causes
Minimal change disease (nephrons appear normal
when viewed with an optical microscope, lesions are
only visible using an electron microscope)
Focal segmental glomerulosclerosis (appearance of
tissue scarring in the glomeruli)
Membranous glomerulonephritis (inflammation of
Aetiology the glomerular membrane)
Membranoproliferative glomerulonephritis
(inflammation of glomeruli along with deposit of
antibodies in their membranes)
Rapidly progressive glomerulonephritis (glomeruli
are present in a crescent moon shape characterized by
a rapid decrease in the glomerular filtration rate)
 oSecondary causes
Diabetic nephropathy
Systemic lupus erythematosus
Syphilis
Hepatitis B (antigens accumulate in the kidney)
Sjögren's syndrome (autoimmune; deposition of
immunocomplexes in the glomeruli)
HIV (viral antigens provoke an obstruction in the
Aetiology glomerular capillary lumen)
Amyloidosis
Vasculitis
Cancer (invasion of the glomeruli by cancerous
cells)
Genetic disorders (altered nephrin: protein in
glomerular filtration barrier)
Drugs (e.g. penicillin, captopril)
 Glomeruli become inflamed
Proteins such as albumin pass through the
cell membrane into the urine.
Hypoalbuminemia results in reduced
oncotic pressure.
Pathophysiology
Edema results
Liver commences compensatory
mechanism involving the synthesis of
proteins, such as lipoproteins resulting
hyperlipidemia.
 Proteinuria
Hypoalbuminemia
Edema
Clinical
manifestations High levels of
cholesterol and other
lipids (fats) in the blood
(hyperlipidemia)
 Puffiness around the eyes
Pitting edema over the legs
Pleural effusion
Pulmonary edema
Clinical Ascites
manifestations Anasarca
Hypertension (rarely) may occur
Anemia due to transferrin loss
Dyspnea
 History
Physical examination
Lab investigations
Diagnosis oUrine analysis (dipstick)
o24 hour urine collection
oKidney biopsy
 Dietary modification
• Low salt
• Restricting fluids
• Protein intake based on kidney condition
Management • Low fat
Edema
• Monitor intake and output
• Daily weighing
• Diuretics
 Monitoring vitals i.e. BP etc
Antihypertensives
• ACE inhibitors
Management • Angiotensin 2 receptor blockers
Balance activity and rest
Treat underlying cause
 New
subtopic Renal failure
 oInability of the kidneys to perform excretory
function
oResult is retention of nitrogenous waste products
oReview of kidney functions:
 Fluid and electrolyte regulation
Introduction  Excretion of nitrogenous waste
 Elimination of exogenous molecules e.g. drugs
 Synthesis of hormones e.g. erythropoietin
 Metabolism of low molecular weight proteins
e.g. insulin
 Acute and chronic renal failure are the two
kinds of kidney failure.
 glomerular filtration declines suddenly (hours to
days)
Acute Renal It is usually reversible
Failure / KDIGO criteria (2012) diagnosed with:
acute kidney • creatinine increase of 0.3 mg/dL in 48 hours,
• creatinine increase to 1.5 times baseline within last
injury 7 days,
• urine volume less than 0.5 mL/kg per hour for 6
hours.
 A persistent impairment of kidney function
Abnormally elevated serum creatinine for
more than 3 months
Chronic Glomerular filtration rate (GFR) less than
Renal 60 ml per minute
Failure Often a progressive loss of kidney function
Renal replacement therapy (dialysis or
transplantation) may be required (end-stage
renal disease)
Glomerular
Filtration
Rate
 Acute
 Prerenal (approximately 60%): Hypotension, volume contraction
(e.g., sepsis, hemorrhage), severe organ failure such as heart failure
or liver failure, drugs like non-steroidal anti-inflammatory drugs
(NSAIDs), angiotensin receptor blockers (ARB) and angiotensin-
converting enzyme inhibitors (ACEI), and cyclosporine
 Intrarenal (approximately 35%): Acute tubule necrosis (from
Aetiology prolonged prerenal failure, radiographic contrast material, drugs
like aminoglycosides, or nephrotoxic substances), acute interstitial
nephritis (drug-induced), connective tissue disorders (vasculitis),
arteriolar insults, fat emboli, intrarenal deposition (seen in tumor-
lysis syndrome, increased uric acid production and multiple
myeloma-Bence-Jones proteins), rhabdomyolysis
 Postrenal (approximately 5%): Extrinsic compression (prostatic
hypertrophy, carcinoma), intrinsic obstruction (calculus, tumor,
clot, stricture), decreased function (neurogenic bladder)
 Chronic
 Diabetes mellitus, especially type 2 diabetes mellitus, is
the most frequent cause of ESRD.
 Hypertension is the second most frequent cause.
 Glomerulonephritis
Aetiology  Polycystic kidney diseases
 Renal vascular diseases
 Prolonged obstruction of the urinary tract, nephrolithiasis
 Vesicoureteral reflux (urine back up into the kidneys)
 Recurrent kidney infections/ pyelonephritis
 Unknown etiology
 History
Detailed present medical illness history
Medical history such as diabetes mellitus,
hypertension
A family history of kidney diseases
Diagnosis Review of hospital records
Previous renal function
Medications especially start date, drug levels of
nephrotoxic agents, NSAIDs
Any use of a contrast agent or any procedure
performed
 Physical examination
Hemodynamics including blood pressure, heart
rate, weight
Volume status, look for edema, jugular venous
distention, lung crackles
Diagnosis Skin: check for any diffuse rash or uremic frost
Look for signs of uremia: asterixis, lethargy,
seizures
Abdomen exam: check for bladder distention,
note any suprapubic fullness
 Laboratory
Urinalysis
Creatinine clearance
Urine electrolytes
 Renal ultrasound
Diagnosis Doppler-flow kidney ultrasound
Abdominal x-ray to Rules out renal calculi
Radionucleotide renal scan, CT scan, and/or MRI
Cystoscopy with retrograde pyelogram
Kidney biopsy
  Treat underlying cause and associated
complications
Intake and output monitoring, daily
weighing
If hyperkalemia with ECG changes, IV
Management calcium, sodium bicarbonate, and glucose
with insulin should be given plus polystyrene
sulfonate to excrete K+. Hemodialysis is also
an emergency method of removal.
If oliguria, restrict fluid (previous day’s
output + 400mls)
 If acidosis: Serum bicarbonate intravenous or per
oral or emergency dialysis
If obstructive etiology present treat accordingly
Management
and or if bladder outlet obstruction secondary to
prostatic hypertrophy may benefit from Flomax or
other selective alpha-blockers
 Severe hyperkalemia
Acidosis
Immediate Volume overload refractory to conservative
dialysis therapy
indications Uremic pericarditis
Encephalopathy
Alcohol and drug intoxications
 Please ask
Thank your
you questions