·
HENOCH-SCHÖNLEIN PURPURA (HSP):
·
BPH
involves prolonged exposure of the prostate gland to androgens. In the
prostate, interactions between epithelial and stromal cells and the extracellular
matrix, mediated primarily by locally produced (intrinsic) growth factors,
appear important. These peptide growth factors,
which include fibroblast growth factors, insulinlike growth factors, and
epidermal growth factors, are felt to be the local forces that determine
prostate growth
mnemonic: AGAR
Abdominal pain
Glomerulonephritis
Arthralgia
Rash
·
Purpura (livedo reticularis) after a
coronary angiogram: think CHOLESTEROL ATHEROEMBOLIC DISEASE
·
Purpura (livedo reticularis) + hepatitis B
+ abdominal pain after meals + footdrop +HTN: think POLYARTERITIS NODOSA
·
THROMBOTIC THROMBOCYTOPENIC PURPURA (TTP):
mnemonic: FAT RN
Pentad:
1. Fever
2. Anemia, microangiopathic hemolytic (+)
schistocytes
3. Thrombocytopenia
4. Renal abnormalities
5. Neurologic abnormalities (confusion,
aphasia,headache, coma, seizures)
·
HEMOLYTIC UREMIC SYNDROME (HUS):
mnemonic: RAT
Renal failure
Anemia, microangiopathic hemolytic
Thrombocytopenia
The FAT RN has TTP and her HUS has
a RAT
TTP and HUS both have
(1) Normal coagulation tests (normal PT/PTT)
(2) Elevated LDH
HUS is
similar to TTP, except that it only affects the RENAL system
·
URINARY CASTS-REVIEW
Normal
RBCS excretion == 2 millions RBCs/day
Hematuria
== 2--5 RBCs Per HPF.
GRANULAR
CAST === Significant renal disease (ARF)
Hyaline
cast === most frequently (M.C.)==normal/mild renal disease.
Epithelial
cast ==== disease affecting tubules/ ATN.
Broadcast
/ Waxy cast === chronic renal disease/CRF, Malignant HTN, Diabetic nephropathy.
RBCs/Dysmorfic(>5%)
RBCs cast == Glomerular injury (kidney) / PSGN.
WBCS
cast == Pyelonephritis
Lipid
cast == Nephrotic synd.
·
Hyperglycemia lowers the plasma sodium
concentration; in the absence of insulin, glucose is an effective osmole that
attracts water from cells and thereby dilutes extracellular sodium. Therefore,
the blood glucose level should always be
examined when a low plasma sodium concentration is being evaluated.
·
In SIADH,
urinary sodium matches intake; as the urine
is usually concentrated, the urinary sodium concentration exceeds 40 mEq/L unless dietary sodium intake is
very low. The urinary osmolality also is inappropriately increased. BUN and
serum uric acid are usually low in patients with SIADH. In patients with
asymptomatic hyponatremia secondary to SIADH, the treatment of choice is fluid
restriction. Administration of normal saline in patients with SIADH can
worsen the hyponatremia. Thiazides block the reabsorption of
sodium and chloride in the distal tubule and can lead to severe
hyponatremia.
·
Creatinine clearance (CCr) can be measured by 24-hour collection of urine, or it
can be estimated through use of a formula that involves the patient's age,
ideal body weight (IBW), and plasma creatinine (Cr): CCr = (140 – age) × (IBW in kg)/(72 × Cr). In females, the
results are multiplied by a correction factor of 0.85.
·
CKD is
defined as either kidney damage or a GFR of less than 60
ml/min/1.73 m2 for longer than 3 months.
The MDRD and Cockcroft-Gault equations provide useful estimates of GFR in
adults.
·
Potassium balance
is generally maintained within normal limits until the GFR falls to less than
10 ml/min. This balance is achieved by an increased potassium excretion rate
per remaining nephron, as well as an increase in extrarenal potassium
excretion, primarily effected via the colon. The development of hyperkalemia
at higher levels of renal function suggests the presence of tubulointerstitial disease or disturbances in the
renin-angiotensin-aldosterone axis.
·
As renal function continues to decline, calcium and phosphorus levels remain within the normal
range initially but at the expense of an ever-increasing level of
PTH. Critical interventions include keeping phosphate levels down, assuring
adequate calcium ingestion, and, if necessary, replacing hydroxylated vitamin
D.
·
The extent to
which urea clearance leads to underestimations of GFR is similar to the extent
to which creatinine clearance leads to overestimations of GFR. Thus, taking the
average of urea and creatinine clearance values will give a very accurate
estimation of GFR.
·
Aggressive
control of hyperglycemia may be more likely to slow progression of renal
disease in patients with type 1 diabetes mellitus than in patients with type 2
diabetes mellitus.
·
ANCA–associated
glomerulonephritis is not associated with staining for immunoglobulin,
complement, or immune deposits.
·
Glucocorticoids
represent the key initial medical therapy for patients diagnosed with FSGS.
·
It is estimated that 10% to 40% of patients with
nephrotic syndrome will develop arterial or venous thromboembolism.
Urinary losses of antithrombin III
are thought to contribute to the pathogenesis of this complication.
·
Patients with IgA
nephropathy typically present with nephritic-like
symptoms that derive from deposition of IgA in the glomeruli. It is the leading
cause of glomerulonephritis worldwide. The male-to-female
ratio is 3:1. The classic presentation in up to 50% of patients with
IgA nephropathy is episodic macroscopic hematuria within 24 hours of a mucosal
infection of the upper respiratory tract. The majority of the rest of patients
with IgA nephropathy present with persistent asymptomatic microscopic
hematuria. This differs from the hematuria of poststreptococcal
glomerulonephritis, which is delayed by 2 to 3
weeks following pharyngitis. The macroscopic hematuria usually
resolves within days.
·
ACE inhibitors
and ARBs should be used cautiously in patients with PAN, because renal involvement may produce a
functional equivalent of classic renal artery stenosis.
·
Plasma ADAMTS
(a disintegrin and metalloprotease with thrombospondin type 1 motif) activity must be severely depressed for TTP to develop. The level of ADAMTS-13
plasma activity is modestly depressed in patients with liver disease,
disseminated cancer, chronic metabolic and inflammatory conditions, and
pregnancy, as well as in newborns. When plasma activity of ADAMTS-13 falls to less than 5% of normal, these large von Willebrand
antigens predominate, bind to platelets, and cause aggregation and thrombi in
small vessels.
Clopidogrel is a thienopyridine (these agents is to prevent ADP-induced platelet aggregation
by irreversibly inhibiting the P2Y12 receptor) antiplatelet agent
that is known to be associated with life-threatening hematologic effects, including neutropenia, TTP, and aplastic anemia.
The true incidence of TTP associated with thienopyridine use is unknown, but it
occurs with both clopidogrel and ticlopidine use. When compared to ticlopidine,
TTP associated with clopidogrel use occurs earlier (often within 2 weeks) and
tends to be less responsive to therapy with plasmapheresis. In addition,
individuals with TTP associated with clopidogrel generally have a higher
platelet count and creatinine and their TTP is less likely to be
associated with ADAMTS13 deficiency. The mortality of TTP
associated with thienopyridines is approximately 25–30%.
·
In patients with Wegener
granulomatosis who are in remission, trimethoprim-sulfamethoxazole
is used to prevent relapse of disease; it is not used in patients with active
disease.
·
Celiac or renal
angiographic findings of microaneurysms
and irregular, segmental constriction of the larger vessels with tapering and
occlusion of smaller intrarenal arteries are diagnostic of classic polyarteritis nodosa.
·
The extent of
renal involvement is the most important prognostic factor in Henoch-Schonlein purpura.
·
Two heavy metals—lead
and cadmium—clearly produce tubulointerstitial
damage.
·
The renal
dysfunction has a negative impact on platelet function.
Desmopressin appears to help with
platelet function. As there is generally an adequate platelet count, platelet
transfusion does not have much impact. Vitamin K is used to help reverse
problems with the extrinsic clotting cascade.
·
Kidney transplant
recipients initially have an increase in mortality, but they have an overall
improvement in long-term survival.
·
Antimetabolites, however, such as azathioprine and mycophenolate mofetil, are
important in immunosuppressive agents in renal transplantation, because of
their lack of nephrotoxicity and because
they have little effect on blood pressure.
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