Renal Pathology: Diseases, Symptoms, and Treatment
Renal Pathology
Filtration is a process that allows the passage of fluid from the glomerulus to Bowman’s capsule by the blood pressure difference between the two areas.
Tubular reabsorption is responsible for recovering useful substances returned to the circulation, allowing toxins to continue their journey through the kidney.
Tubular secretion maintains the normal acid-base balance: reabsorption of filtered bicarbonate and excretion of protons.
Disease Etiology
Infection, immune, or intraglomerular intravascular coagulation, metabolic, neoplastic, drugs and toxic, vascular, hereditary.
Symptomatology
Dysuria, frequency, burning urination, urgency, voiding latency, polyuria, nocturia, nephrotic colic.
Urinary Tract Infections
- Urinary tract infections (UTI) are the most common infectious complication during pregnancy, and their incidence ranges from 3 to 12%.
- Almost all infections are acquired through up-colonization of the urethra and bladder, and eventually, they climb down the ureters into the kidney.
- UTI can occur in 3 ways:
- Asymptomatic bacteriuria
- Lower Tract Infection: Uterine or acute cystitis (features of dysuria, polyuria, burning urination, and urinary urgency. Macroscopic hematuria is sometimes present.)
- Upper urinary tract infection or acute pyelonephritis
Urolithiasis
Renal Lithogenesis (I)
Salts of calcium (70%), oxalate, uric acid (5%), magnesium-ammonium phosphate or struvite (20%), cystine (<1%).
Types
- Calcium stones: May be accompanied by hypercalciuria associated with hyperuricosuria, hyperoxaluria, hypocitraturia, or without known metabolic abnormalities (idiopathic calcium stones).
- Uric lithiasis: 10-25% of patients with gout, acid and pH, hyperuricosuria.
Renal Lithogenesis (II)
Factors
- Presence in urine of the components in higher concentration than normal.
- Decreased protective components of urine.
- Urine pH: solubility precipitates uric acid = acidic pH, struvite = alkaline pH.
Types
- Lithiasis Cystine: Amino acid disturbance that affects metabolite transport into the cell membrane of the renal tubule and intestinal epithelium of four essential amino acids (cystine, ornithine, lysine, and arginine).
- Struvite urolithiasis: Only when the urine is infected by ureolytic germs. Large stones acquiring the shape of the pelvis and calyces (coralliform calculations).
Renal Lithogenesis (III)
Predominant form when the factors that promote lithogenesis are greater than those that inhibit it.
Renal Colic (I)
Most common cause: migration of stones from the pelvis to the bladder, or blood clots.
Characteristics of pain
- Lumbar or iliac fossa.
- To the external genitalia and inner thigh: if the obstacle has progressed and radiates along the course of the ureter.
- Paroxysmal exacerbations.
Renal Colic (II)
Forms: vegetative (nausea, vomiting, ileus), gross hematuria (if the ureteral mucosa is eroded by the calculus), stirring motor (no relief at any position).
Differential Diagnosis: Acute appendicitis, biliary colic, acute diverticulitis, acute pancreatitis, gynecologic processes (ectopic pregnancy, adnexitis, torsion of an ovarian cyst).
Diagnostic methods: Simple renal X-ray, ultrasound, intravenous pyelography, computed tomography (CT).
Acute Renal Failure
Rapid loss of glomerular filtration and tubular function leading to an imbalance in the metabolism of water, electrolytes, and solutes. It may be superimposed on chronic renal failure (CRF) of multifactorial origin. Oliguric (60-80%) urine output <400 cc/day. Non-oliguric (20-40%).
Pre-Renal Acute Renal Failure
Hypovolemia: bleeding, burns, third spaces, gastrointestinal and renal loss. Hypotension: septic shock, cardiogenic. Edematous states: congestive heart failure (CHF), decompensated hepatic cirrhosis (DHC), lipoid nephrosis. Renal hypoperfusion: renovascular stenosis, renal artery thrombosis, nonsteroidal anti-inflammatory drugs (NSAIDs).
Intrinsic Renal Acute Renal Failure
Tubular Disease Acute Ischemic (prolonged hypoperfusion), nephrotoxins. Rapidly progressive glomerulonephritis (GN): vasculitis, Goodpasture syndrome. Acute interstitial nephritis: drugs, acute pyelonephritis. Vascular Disease: thrombotic microangiopathy, cholesterol embolization.
Obstructive Acute Renal Failure
Pelvis: Renal lithiasis, papillae. Ureter or ureter in solitary kidney: carcinoma, kidney, blood clots, tubal. Bladder neck: prostatic enlargement (benign or malignant), bladder carcinoma. Urethra stricture.
Acute Tubular Disease
Most common cause: ischemic, nephrotoxic.
Acute Renal Failure Oliguria
Glomerular filtration and intrarenal blood flow. Tubular cell injury, obstruction, and retrofiltration.
Hypoperfusion – Fall in Glomerular Filtration
Under 80 mm Hg mean arterial pressure (MAP), intense vasoconstriction (endothelin, angiotensin II), mesangial contraction (<area and <glomerular filtration coefficient), minor endothelial nitric oxide (NO) production, intratubular obstruction, and backscatter.
Serious Consequences of Acute Renal Failure
Acute oliguria, pulmonary edema, uremic syndrome, hyperkalemia, metabolic acidosis, disturbances of calcium/phosphorus.
Reversible Causes of Uremic Symptoms
Lupus, vasculitis. Diet: protein. Hypercatabolism: steroids, infection. Metabolic: acidosis, hypercalcemia.
Acute Renal Failure Treatment Factors Potentially Reversible
Hypovolemia, hypotension, accelerated hypertension, nephrotoxic agents, UTI or systemic infection, urinary tract obstruction.
Acute Renal Failure Dialysis Indication
Absolute: severe uremic syndrome (pericarditis). Otherwise unmanageable: hypervolemia, severe hyperkalemia, metabolic acidosis.
Chronic Renal Failure
- Consequence of progressive deterioration of renal function.
- Decreased glomerular filtration rate (GFR).
- Numerous cases and is associated with a variable speed up to renal failure (end-stage renal failure – ESRF).
- End-stage renal failure: clinical characteristic (uremic syndrome), which spontaneously evolves to death since one can only survive with hemodialysis or transplantation.
Causes of ESRF
a) Glomerulopathies b) Hypertensive nephropathy (nephrosclerosis) c) Inherited diseases: polycystic kidney d) Chronic interstitial nephritis e) Obstructive uropathy and urinary tract infection.
Pathophysiology
- The irreversibility of the damage in some nephrons.
- The adaptation of the remaining nephrons (hyperperfusion) (hyperfiltration).
Affects Tubular Function
Increased tubular secretion. Thus, cellular metabolism resulting substances such as creatinine, urea, and uric acid are retained, increasing their concentration in the bloodstream.
- The progression of nephropathy partially reduced GFR often progress to end in CRF.
Stages of Chronic Renal Failure
Reduced Renal Reserve
The patient is asymptomatic, although the GFR has fallen to 60-70%.
Early Renal Insufficiency
The GFR is between 20-50% of normal, and symptoms appear first: asthenia, anemia, and mild elevation of blood urea nitrogen (BUN) (20-30mg/dl).
Established Renal Failure
The GFR is reduced <10-20%. Laboratory abnormalities appear frank.
End-Stage Renal Failure
Uremic syndrome: GFR <10%. Symptoms and signs: cardiovascular, digestive, nervous, cutaneous, endocrine, skeletal muscle.
Multiple myeloma, diabetic nephropathy, amyloidosis, polycystic kidneys.
Factors Corrected Would Delay the Course of CRF
Urinary tract obstruction, hypertension, diabetes mellitus, use of nephrotoxic drugs such as aminoglycoside antibiotics and nonsteroidal anti-inflammatory drugs, overload of solutes such as proteins, which may contribute to hyperfiltration, dehydration. Heart failure, as spending under reduced renal perfusion and increases nitrogen retention.
Uremic Syndrome
This name is given to all symptoms and signs accompanying nitrogen retention (uremia) characteristic of chronic renal failure.
Coronary heart disease in these patients is the leading cause of death.
Gastrointestinal
Anorexia, nausea, and vomiting, these symptoms improve with the restriction of dietary protein and dialysis. Gastrointestinal bleeding from peptic ulcer or gastritis.
Hematologic and Immunologic
a) Anemia. Appears when the GFR is reduced to 30-40 ml/min. It is multifactorial: erythropoietin deficiency, shortened red cell life, malnutrition (reduced intake of iron, folate), and bleeding. Anorexia’s own urea syndrome contributes to this trend.
b) Hemostasis. Prolongation of bleeding, by platelet dysfunction.
c) Immune Response. Immunocompromised patients are more susceptible to infections such as pneumonia and sepsis.
Water and Electrolyte Metabolism
Nephropathic patients lose the ability to concentrate and dilute urine. As a result, urinary osmolality and plasma are very similar. Potassium metabolism. Acid-base balance. When GFR <20 ml/min, the nephron proton secretion is insufficient => metabolic acidosis. Metabolism of calcium and phosphorus is altered early in chronic renal failure (with GFR halved). Become symptomatic only in the terminal stages.
Neurological and Psychiatric Disorders
These are mental impairment, abnormal movements, and involvement of peripheral nerves. The commitment includes impairment of memory, the ability of abstraction, and then lethargy, drowsiness, and uremic coma.
Endocrine and Growth
They are especially important in children and women of childbearing age. They include thyroid and gonadal dysfunction. Renal failure slows growth, partly by malnutrition (concomitant anorexia) and renal osteodystrophy.
Arterial Hypertension
Hypotension can compromise the blood supply to tissues and vitality, especially the heart, brain, kidney, and retina.
Arterial hypertension (AHT) can be life-threatening when sudden and rapid installation, you can create irreparable damage and death in the same organs mentioned.
Chronic Hypertension
It is the second leading cause of medical consultation and medication use.
Its importance lies in two facts.