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Alterations of Renal and Urinary Tract Function Concept Maps

Gary L. Schofield, RN

Potential Causes & Process of Renal Failure


Renal Cancer




Renal Failure

-Reverses - Abrupt renal functions

Progressive/ Irreversible

End Stage Renal Disease

Impaired Renal Blood Flow

Complete Renal Failure GFR gradually Intra renal Acute tubular necrosis Acute glomerulonephritis Renal Vascular Obstruction Cortical Necrosis Allograft Rejection Transplant Post renal Kidney Stones Neoplastic Disease Nephrons destroyed

Pre renal (Renal Ischemia) Shock CO Anaphylaxis

Remaining Nephrons Workload -Hypertrophy - ability to concentrate urine


Bladder = infection



Wilms Tumor

Hydroureter Hydronephrosis

Bladder = Acute or Chronic Renal Failure

Embryonal Tumor Nephroblastoma Sporadic and inherited origins Associated with other anomalies

Lower Urinary Tract Obstructions Kidney Stones Neurogenic Bladder

Bladder Neck Dyssynergia Interruption of nerve supply Prostate Enlargement

Urethral Stricture

Severe Pelvic Organ Prolapse

Most common in pelvis of kidney Calcium or Phosphate 7580 % of the time

Gender Race Geographic Location Seasonal Factors Fluid Intake Diet Occupation

Upper Motor Neuron Lesion

Lower Motor Neuron Lesion

Loss of Voluntary control of voiding

Loss of voluntary and involuntary control of voiding

Congenitally abnormal ureter Reflux of urine from bladder to kidney Infection, renal scarring, pyelonephritis

Vesicoureteral Reflux

Caused By Bacteria, Fungal and Parasite



Virulence of Uropathogens
Most Common Site for UTI Bacterial Attaches to Uroepithelium Bacteria Form Biofilm

Host Defense Mechanisms

Periurethral Mucus Secreting Gland


Sphincter Mechanisms Chronic

Causes: E. Coli, Klebsiella, Pseudomonas, Staph

Body Immune System (Bladder Wall)

Infection initiates inflammatory response

Association: Tobacco Use, Obesity, Long-term Analgesic use

Common Causes: Kidney Stones Vesicoureteral Reflux Pregnancy Neurogenic Bladder Instrumentation Female Sexual Trauma

Bladder Tumors Renal Adenoma Renal Cell Carcinoma

Primary Associated with mutation of gene P53


Benign Tumors Located near cortex of kidney

Most common renal neoplasm Proximal tubule epithelial cells

Increase Risk Workers exposed to chemicals, rubber, & in textile industry

Result of invasion of cancer from bordering organs

Smokers (men)


Common Cause: E Coli


Infection of renal pelvis and interstutium

Recurrent Autoimmune Infections

Common Causes Kidney Stones Vesicoureteral Reflux Pregnancy Neurogenic Bladder Instrumentation Female Sexual Trauma

Inflammatory Process damages tubular cells

Inflammation and scarring of kidney Pelvis, calyces dilated & blunted

Destruction of tubules Areas of atrophy/dilation/ diffuse scaring

Usually localized abscesses Healing occurs Deposition of Scar tissue Atrophy of affected tubules

Impairment of function Urine-concentration ability affected

Excretion of diluted urine

Affects primarily the pelvis, calyces, and medulla Rarely causes renal failure

Renal Failure

Glomerular Disorders
Acute Glomerulonephritis S/S Hematuria Red Blood Cell Casts Protenuria GFR Oliguria Edema HTN Abrupt onset 7-10 after infection Group A Strep S/S 10-21days after infections

IgA Nephropathy Berger Disease

Nephrotic Syndrome

Crescentic Glomerulonephritis (Rapidly Progressive)

Most Common Form Most individuals Children recover with minimal loss of renal function Disturbance in Glomerular Basement Memb (metabolic, biochemical, physiochemical) leads to increase permeability to protein

Chronic Glomerulonephritis

Several Glomerular Diseases

Idiopathic Proliferative glomerular diseases

Unknown cause 24-48 hrs after URI or GI infection

Focal or Diffuse Segmental fibrosis and deterioration

Antiglomerular Basement Membrane (Good-pasture Syndrome) Prognosis variable 20-50% progress to Renal Fail





Tubular dilation and atrophy Cause: Immune response Toxin/Drugs Vasc. Disorders Damage: Biochemical Mediators of Inflammation Complement activation Neutrophils/Monocytes Poor Prognosis

Example of Crescent Glomerulonephritis


Antibody Formation Affects: Pulmonary Capillary Glomerular Basement Membs

Poor Prognosis

Treatment: Normal, Low-fat Diet; Salt Restriction Diuretics; Antigoagulants; Removal of toxins; Steroids; Albumin Replacements

Renal Failure

Structural Abnormality Hypospadias

Congenital condition in which the urethral meatus is located on the ventral side of the penis

Related to disruption in male hormones Accompanied by Chordee or penile torsion Corrective Surgery

Epispadias Exstrophy of Bladder

Exstrophy of the bladder- Urethral opening on the dorsal surface of penis.

Urethral opening small and situated behind the glans with fissure extending the length of penis Constant dribbling of urine Caused by intrauterine failure of the abdominal wall and the mesoderm of the anterior bladder to fuse Reconstructive surgery girls teens Boys 2-3 yrs of age Intrinsic malformation of smooth muscle or urothelial development produces obstruction in 90% of cases. Causes kinking and scarring Polyps rarely arise form the prostatic urethra often cause sever obstruction and impair renal embrogenesis leading to UTI, Vesicoureteric reflux, and renal failure. Resection as soon as possible Associated with a functional or organic obstruction of the collecting system Obstruction may begin prior to birth

Extensive congenital anomaly in which the lower urinary tract is exposed directly to the surface of the body

Ureteropelvic Junction Obstruction Bladder Outlet Obstruction Hypoplastic(Dysplastic Kidneys

Blockage of the tapered point where the renal pelvis transitions into the ureter

A urethral valve is a thin membrane of tissue that occludes the urethral lumen and obstructs urinary outflow in males.

Ureteric duct grows into the metanephric tissue, triggering the formation of the kidneys in utero. If this growth does not occur the kidney is absent or hypoplastic (small) Renal dysplasia results from abnormal differentiation of renal tissue Absence of one or both kidneys Potter syndrome (bilateral renal agenesis) Autosomal dominant inherited disorder PKD-1 and PKD-2 mutations account for the disease

Renal Agenesis Polycystic Kidneys

Clearly hereditary Bilateral agenesis is usually fatal Unilateral males more affected The gene products regulate epithelial growth and differentiation.

Corwin, E. J. (2000). Handbook of Pathophysiology (2nd ed.). Philadelphia, PA: Lippincott. Gray, M., Huether, S., & Forshee, B. (2006). Alterations of renal and urinary tract function. In K. L. McCance & S. Huether (Eds.), Pathophysiology: The Biologic Basis for Disease in Adults & Children (pp.1301- 1336). St Louis, MO: ElSevier Mosby. Huether, S. (2006) Alteration of renal and urinary tract functions in children. In K. L. McCance & S. Huether (Eds.), Pathophysiology: The Biologic Basis for Disease in Adults & Children (pp.1337- 1351). St Louis, MO: ElSevier Mosby.