Renal Diseases Flashcards
What are the four classification/type of Renal Diseases?
GLOMERULAR
TUBULAR
INTERSTITIAL
VASCULAR
Most often are Immune-Mediated
Glomerular
Result from INFECTIOUS or TOXIC SUBSTANCES
TUBULAR and INTERSTITIAL
Causes a Renal Perfusion that subsequently induces both MORPHOLOGIC and FUNCTIONAL changes in the kidney
VASCULAR
Increased permeability of the Glomeruli to the passage of Plasma Proteins [Albumin]
NEPHROTIC SYNDROME
[3.5 g/day]
HEAVY PROTEINURIA
[Plasma Albumin usually <3 g/dL →Liver Synthesis unable to compensate for the large amount of protein excreted in the urine]
HYPOPROTEINEMIA
HYPERLIPIDEMIA [Increased Plasma Levels of:
▪ Triglycerides
▪ Cholesterol
▪ Phospholipids
▪ VLDL
One Cause: Post-Streptococcal Infection → Known as: Acute Poststreptococcal Glomerulonephritis [Group A Beta Hemolytic Streptococci – those with M PROTEIN in their cell wall induces this type of Nephritis
ACUTE GLOMERULONEPHRITIS
Post-Streptococcal Infection → Known as:
Acute Poststreptococcal Glomerulonephritis
BLOOD: Elevated ASO Titer
ACUTE GLOMERULONEPHRITIS
Non-AGN: Non-Streptococcal Agent
ACUTE GLOMERULONEPHRITIS
Bacteria: Pneumococci
ACUTE GLOMERULONEPHRITIS
Viruses: Mumps, Hepa B
ACUTE GLOMERULONEPHRITIS
Parasitic Infection: Malaria
ACUTE GLOMERULONEPHRITIS
SCLEROSIS of the Glomeruli
FOCAL SEGMENTAL GLOMERULONEPHRITIS
FOCAL: Occurring in some Glomeruli
FOCAL SEGMENTAL GLOMERULONEPHRITIS
SEGMENTAL: Affecting a Specific Area of the Glomerulus
FOCAL SEGMENTAL GLOMERULONEPHRITIS
PREDOMINANT FEATURE: Proteinuria
FOCAL SEGMENTAL GLOMERULONEPHRITIS
Characteristics:
Cellular Proliferation of the MESANGIUM
MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS
Characteristics:
LEUKOCYTES INFILTRATION
MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS
Characteristics:
Thickening of the Glomerular Membrane
MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS
Characteristics of MEMBRANOPROLIFERATIVE GLOMERULONEPHRITIS:
▪ Cellular Proliferation of the MESANGIUM
▪ LEUKOCYTES INFILTRATION
▪ Thickening of the Glomerular Membrane
Most prevalent type of Glomerulonephritis worldwide
IgA NEPHROPATHY
Deposition of IgA in the Glomerular Mesangium
IgA NEPHROPATHY
Development: Slow and Silent
CHRONIC GLOMERULONEPHRITIS
80%: Have previously some form of Glomerulonephritis
CHRONIC GLOMERULONEPHRITIS
20%: Forms of Glomerulonephritis that has been unrecognized
CHRONIC GLOMERULONEPHRITIS
Destruction of RENAL TUBULAR Epithelial Cells
ACUTE TUBULAR NECROSIS
What are the 2 Distinct type of Acute Tubular Necrosis?
ISCHEMIC and TOXIC
Follows a HYPOTENSIVE event that result in decrease perfusion of the kidneys followed by a renal tissue ischemia
Ischemic ATN
The 3 Principal Causes of ISCHEMIC ATN are?
▪ Sepsis
▪ Shock
▪ Trauma
Results from exposure to NEPHROTOXIC AGENTS
TOXIC ATN
Caused by Variety of agents separated into Categories: TOXIC ATN
ENDOGENOUS NEPHROTOXIN and EXOGENOUS NEPHROTOXIN
Normal solutes or substances that become toxic when their concentration in the bloodstream is excessive
ENDOGENOUS NEPHROTOXIN
Hemoglobin→Hemoglobinuria→Severe Hemolytic Events
Myoglobin → Myoglobinuria → Rhabdomyosis
Uric Acid
Immunoglobulin Light Chain
ENDOGENOUS NEPHROTOXIN
Substances ingested or absorbed
EXOGENOUS NEPHROTOXIN
These are EXOGENOUS NEPHROTOXIN substances that are absorb:
▪ Therapeutic agents
▪ Anesthetics
▪ Radiographic Contrast Media
▪ Chemotherapeutic Drugs
▪ Recreational Drugs
▪ Industrial Chemicals
Impaired ability to reabsorb GLUCOSE
Renal Glucosuria
Impaired ability to reabsorb specific AMINO ACIDS
Cystinuria [Cystine and Dibasic AA] and
Hartnup Disease [Monoamino- Monocarboxylic AA]
Impaired ability to reabsorb SODIUM
Bartter’s Syndrome
Impaired ability to reabsorb BICARBONATE
Renal Tubular Acidosis Type II
Impaired ability to reabsorb CALCIUM
Idiopathic Hypercalciuria
Excessive reabsorption of CALCIUM
Hypocalciuric Familial Hypercalcemia
This proximal tubular dysfunction that has an excessive reabsorption of SODIUM
Gordon’s Syndrome
Excessive reabsorption of PHOSPHATE
Pseudohypo Parathyroidism
Generalized LOSS OF PROXIMAL TUBULAR FUNCTION
Not reabsorbed from the Ultrafiltrate and excreted in the Urine:
▪ Amino Acid
▪ Glucose
▪ Water
▪ Phosphorus
▪ Potassium
▪ Calcium
Fanconi Syndrome
Impaired ability to reabsorb PHOSPHATE
Familial Hypophosphatemia [Vitamin D Resistant Rickets]
This is both Proximal and Distal Tubular Dysfunction
Idiopathic Hypercalciuria
Impaired ability to ACIDIFY URINE
Renal Tubular Acidosis, Types I and IV
Impaired ability to retain SODIUM
Renal Salt-Losing Disorder
Impaired ability to concentrate URINE
Nephrogenic Diabetes
This distal tubular dysfunction that has excessive reabsorption of SODIUM
Liddle’s Syndrome
Inability to reabsorb INORGANIC PHOSPHATES
Renal Phosphaturia
These are the Proximal Tubular Dysfunctions
Renal Glucosuria
Cystinuria [Cystine and Dibasic AA]
Hartnup Disease [Monoamino- Monocarboxylic AA]
Bartter’s Syndrome
Renal Tubular Acidosis Type II
Idiopathic Hypercalciuria
Hypocalciuric Familial Hypercalcemia
Gordon’s Syndrome
Pseudohypo Parathyroidism
Fanconi Syndrome
These are the Distal Dysfunctions
Familial Hypophosphatemia [Vitamin D Resistant Rickets]
Idiopathic Hypercalciuria
Renal Tubular Acidosis, Types I and IV
Renal Salt-Losing Disorder
Nephrogenic Diabetes
Liddle’s Syndrome
Renal Phosphaturia
LOWER UTI
Urethra:______
Urethritis
LOWER UTI
Bladder:______
Cystitis
▪ Painful urination:______
▪ Burning Sensation
▪ Frequent urge to urinate
Dysuria
Lower UTI:
Urethritis
Cystitis
Dysuria
UPPER UTI
Renal Pelvis alone:______
Pyetitis
UPPER UTI
Renal Pelvis including Interstitium:______
Pyelonephritis
What are the Bacterial infection that involves in ACUTE PYELONEPHRITIS?
▪ Renal Tubules
▪ Interstitium
▪ Renal Pelvis
MECHANISM:
1. Movement of bacteria from the lower urinary tract to the kidney
2. Localization of the bacteria from the bloodstream in the kidneys [Hematogenous infection]
ACUTE PYELONEPHRITIS
Develops when permanent inflammation of renal tissue causes permanent scarring that involves the:
▪ Renal Calyces
▪ Pelvis
CHRONIC PYELONEPHRITIS
Allergic response to the interstitium of the kidney
ACUTE INTERSTITIAL NEPHRITIS
Most Common Cause: Acute Allograft Rejection of a Transplanted Kidney
ACUTE INTERSTITIAL NEPHRITIS
Normal flora of GIT and Vagina
Candida species [e.g. Candida albicans]
Proliferation of yeasts due to:
▪ Changes in pH
▪ Adversely disrupted by antibiotics
Clinically Sudden:
▪ Decrease of GFR
▪ Azotemia
▪ Oliguria [Urine Output of <400MI]
ACUTE RENAL FAILURE
Results from Decrease Renal Blood Flow [25% of cases]
Urine Sodium Concentration is Low = Incresed amount of Sodium being reabsorbed
PRE-RENAL
Approximately 65% of cases Renal Damage
Can result from:
▪ Glomerular
▪ Tubular
▪ Vascular Disease Process
Increased Urinary Excretion of Sodium
RENAL
Approximately 10% of cases
Obstruction in the urine flow
POST RENAL
Calculi “Stones”
Renal Catalyces
Pelvis
Bladder
Ureter
Calcium
75%
Calcium with Oxalate
35%
Calcium with Phosphate
15%
Calcium with others
25%
Magnesium Ammonium Phosphate
15%
Uric Acid
6%
Cystine
2%