Renal parenchyma

In acute uric acid nephropathy, acute renal failure occurs as a result of blockage of urine flow secondary to massive precipitation of uric acid crystals in the collecting ducts and ureters. This syndrome is a well-recognized complication in patients with myeloproliferative or lymphopro-liferative disorders and results from massive malignant cell turnover, particularly after initiation of chemotherapy. Chronic urate nephropathy is caused by the long-term deposition of urate crystals in the renal parenchyma. 

Vectors can be injected into the kidney at the location of choice or at multiple sites either beneath the capsule or into the renal parenchyma. The disadvantage of this technique is that the transgene expression is limited to renal tissue surrounding the needle track and the needle penetration per se can cause cell damage. This approach could be relevant for localized renal tumors where anti-angiogenic, pro-apoptotic, or tumor-suppressive genes could be injected. 

Urokinase (UK) was the first of the thrombolytic agents to appear in widespread use in the 1990s (20). UK is a naturally occurring thrombolytic produced by renal parenchyma and is therefore found in human urine. It has a plasma half-life of 15 minutes and when administered intravenously, it is rapidly removed from circulation by hepatic clearance. 

This patient, who had autosomal dominant polycystic kidney disease (ADPKD), almost drowned and then developed ALPE. On July 20, 1990, he nearly drowned in the sea at 1500 hours, and was brought to our hospital by ambulance for dyspnea and severe loin pain at 1620 hours. On admission, metabolic acidosis was observed. His CRP, serum creatinine, CPK, amylase, and urinary protein levels were 1+, 1.5mg/dl, 116 U/l, 592IU/1 (derived from the salivary gland), and 2+, respectively. His body temperature was 37.7°C, and his blood pressure was 110/60 mmHg. His pulse and respiratory rate were 120/min and 22/min, respectively. Delayed CT 6h after the administration of contrast medium showed wedge-shaped contrast enhancement in the noncystic renal parenchyma (Fig. 34). On July 24, a bone scan with MDP revealed patchy lesions (Fig. 35). His serum creatinine level was 1.3 mg/dl, which had decreased to 1.0 mg/dl on July 27. The patient was then discharged. 

Fig. 34. Delayed CT 6h after the administration of contrast medium to an autosomal dominant polycystic kidney disease (ADPKD) patient with ALPE. Top. Wedge-shaped contrast enhancement can be seen in the noncystic renal parenchyma region at onset. Bottom. CT under the same conditions in the recovery phase did not show wedge-shaped contrast enhancement...

Braedel HU, Schindler E, Cullen P, Hoene E (1987) Demonstration of residual contrast medium in renal parenchyma using computerized tomography. J Urol 137 11-14... 

From our investigation it is evident that abnormal excretion of tryptophan metabolites is not a typical feature of bladder tumor subjects, since human beings with neoplastic and nonneoplastic extrabladder urinary diseases have also been found to excrete spontaneously elevated amounts of tryptophan derivatives. It seems that the metabolic abnormality is not restricted to bladder tumors, but is rather more specific for patients with tumors of the upper urinary tracts and of the renal parenchyma. Actually 59% of these patients (Fig. 4) excreted abnormal amounts of kynurenine, 3-hydroxykynurenine, and 3-hydroxyanthranilic acid. 

Dose and length of therapy with loop diuretics may predict the likelihood of developing calcium deposits in the renal parenchyma. Ten premature infants developed nephrocalcinosis after receiving furosemide at a dose of at least 2 mg/kg per day for 12 days [102]. In a study by Saarela et al, infants who developed renal calcifications were receiving higher daily doses of furosemide than infants who had not developed this complication (1.9 + 0.6 vs. 1.3 + 0.4 mg/kg per day p value-0.01) [104]. Calcifications were diagnosed within a few months of initiating furosemide. 

Regarding renal disease, the largest study to date has shown that CHF is more common in patients with advanced chronic renal disease, with BNP levels independently associated with CHF. At present, however, hemodialysis appears to influence the optimum cutoff concentration for BNP and NT-proBNP in the diagnosis of CHF, with advanced stages of renal disease showing higher cutoff values. BNP and NT-proBNP are secreted in a pulsatile fashion from cardiac ventricles with an approximate half-Ufe for BNP of 22 minutes in blood, with the NT-proBNP half-life on the order of hours. While one mechanism of BNP clearance involves the renal parenchyma, the kidney is not thought to be the... 

Prerenal ARF results from hypoperfusion of the renal parenchyma, with or without systemic arterial hypotension. Renal hypoperfusion with systemic arterial hypotension may be caused by a decline in... 

The release of some of these mediators attracts inflammatory cells such as macrophages, neutrophils, and T cells to the renal parenchyma, in addition to platelets. The consequence of infiltration of the renal parenchyma by these inflammatory cells and platelets is the activation of glomerular cells to produce mitogenic or growth factors. 

After intravenous infusion of iron containing drugs or in cases of chronic iron overload in chronic diseases, a change in the bone-to-kidney ratio of diphosphonate complexes has been reported, namely, a decrease in bone uptake and an increase in accumulation in renal parenchyma (McRae et al. 1976). Dissociation of the Tc-diphos-phonate complex and a conversion into the renaltropic gluconate was proved in the presence of ionic iron(II) and calcium. In vivo alteration of the complex was concluded from an increase in renal uptake even after infusion of dextrose. 

For static imaging of the kidneys, the radiotracer is retained in the renal parenchyma hy tubular fixation. The scintigram shows solely functional parenchyma. Necrotic tissue and inflammatory processes are not imaged a tumor, cyst or abscess appears as cold area. 

After intravenous injection, the Tc(III)-DMSA complex is taken up in the renal parenchyma (24% at 1 h), showing high cortical affinity (Lin et al. 1974). Uptake is related to renal cortical perfusion the plasma clearance half-time in patients with normal kidney function is 56 min (Enlander et al. 1974). 

---